A Divided Community
In a September 2025 Viewpoint published in Nature Metabolism entitled “Mitochondria Transfer,” the editors noted, “. . . the topic continues to be met with skepticism.” As a result, the journal asked nine mitochondrial biologists to share their personal views on intercellular mitochondria transfer. There was little new here.
Their responses amounted to yes, no, and maybe. Many questions loom for otherwise promising results. What are the mechanisms and consequences of this process? If mitochondria do move between cells endogenously, when they arrive in another cell, do they resume their normal functions? Does the transfer of a relatively small number of mitochondria have the power to rescue a cell that is under bioenergetic stress?
At MitoWorld, we know most of the Viewpoint respondents, and we know the gulf between them. By kicking off debate, Nature Metabolism has started a process that we hope can mature from rhetoric to a more evidence-based picture of the efficacy of mitochondrial transfer and transplantation. Across the globe, investigations are underway in both categories. Given the limited mechanistic understanding of this process, it is surprising that mitochondrial transplantation is now a not uncommon medical intervention and remains a tantalizing subject of research and development in a variety of biotech companies.
First Step: Nomenclature
In all of this, there is a blurring of terminology. In January, Jon Brestoff and Keshav Singh, et al. published “Recommendations for mitochondria transfer and transplantation nomenclature and characterization,” also in Nature Metabolism. What is clear in their paper’s title is the notion of i) transfer being endogenous, part of an intrinsic biological mechanism and ii) transplantation, the act of deliberately introducing mitochondria into organs, tissues, and cells being exogenous. Over 30 researchers participated in what was a laudable effort to explore agreed-upon naming, processes, and explanatory conventions. While the consensus statement and an agreement for an International Committee on Mitochondria Transfer and Transplantation Nomenclature (ICMTTN) represents an important step forward, notable disagreements persist. Foremost among the complications related to mitochondrial transfer and transplantation relates to the unknown fate of any mtDNA harbored by incoming organelles.
Second Step: Conference
MitoWorld found itself in the middle of this controversy when it was asked to help with the first Mitochondrial Transplantation Conference. Held in April at Hofstra University, the event was organized by Northwell Health and led by Lance Becker. It featured a mix of compelling medical intervention talks and video for failing hearts (James McCully), treatment for stroke victims (Melanie Walker), and other resuscitation experiments with animals (Lance Becker). MitoWorld assisted in having endogenous transfer represented (Jonathan Brestoff). In all of this, there was excitement but also apprehension that parents of children and adults with mitochondrial genetic diseases will be given false hope for near-term treatments. Several drug developers were present, as were patient groups. It is likely some form of transplantation organization will emerge from that meeting.
Deeper Dive—Transfer and Transplantation
Given the lack of evidence-based dialogue, MitoWorld reached out to the Viewpoint respondents who are actively doing work in both categories. Yasemin Sancak, The Sancak Lab, University of Washington Pharmacology, and Rubén Quintana-Cabrera, Neurometabolism and Mitochondrial Dynamics Lab, Instituto Cajal, CSIC responded to MitoWorld.
MitoWorld: Why do you think there is such a controversy about mitochondria transfer and transplant?
Sancak: Transfer of mitochondria between cells is shown in different organisms and systems, and although this is relatively novel finding, it is widely accepted in the field. However, mitochondria transplantation attracts skepticism. In my opinion, the controversy stems from the expectation that, for mitochondrial transplantation to work as intended, the transplanted mitochondria should successfully incorporate into the host tissue in large numbers and maybe survive there for a long time, integrate into the donor tissue, and restore mitochondrial function and tissue health. Currently, the evidence of this happening is limited, and mechanisms of mitochondrial entry and survival are not well understood. But we also cannot ignore the exciting data that show the utility of mitochondrial transplantation in the clinic. Until we understand the molecular details and mechanisms of this process, the controversy is likely to continue. The field needs more preclinical and clinical research to understand mechanisms of therapeutic benefit and to establish clinical guidelines.
Quintana-Cabrera: These are quite novel concepts, now widely accepted by the scientific community after solid data in different cells and tissues. My perception is that both general and even specialized audiences are mostly focused on the incorporation of healthy mitochondria from neighboring cells or tissues to enhance mitochondrial activity in the compromised recipient cell. However, we should not overlook the transfer of damaged mitochondria, which may also benefit a cell by enabling their elimination through surrogate degradation in neighboring cells. Regarding transplants, the apparent controversy mainly concerns the injection of isolated mitochondria. Transplants using donor cells, such as mesenchymal stem cells or mitochondria encapsulated in vesicles or artificial membranes are viewed as able to better withstand the extracellular environment and the journey through the body to the target tissue. However, those advocating for transplants of isolated mitochondria need to standardize the approaches and to clarify how mitochondria survive outside the cell, influence inflammation, and integrate into recipient cells, or if they can take over native mitochondrial function in the long term.
MitoWorld: What may convince you that transfer happens naturally and/or that transplantation has effects?
Sancak: Many animal and cell culture studies show that mitochondrial transfer happens naturally, and this process is likely to serve different functions. Mitochondrial transplantation research in a pre-clinical setting mostly shows positive outcomes, but the long-term benefits of mitochondrial transplantation are not addressed. A small number of human studies show clinical benefit, but these are mostly feasibility and safety studies that were conducted with a small number of patients. One promising common finding from human studies so far is that mitochondrial transplantation does not seem to have any adverse effects and is generally considered to be safe. I think this is very promising and should open the door to bigger clinical trials. Ultimately, well-controlled clinical trials are needed to determine if mitochondrial transplantation will work for a disease of interest and what long term effects will be.
Quintana-Cabrera: A growing body of evidence demonstrates the natural occurrence of different types of transfer, mediated by tunneling nanotubes, microvesicles, or naked mitochondria, across various tissues and both in physiology and pathology. This is leading the scientific community to accept mitochondrial transfer as a naturally occurring event.
Of course, this is still a young field, and existing gaps need to be addressed by thoroughly evaluating the various dimensions of mitochondrial transfer. For example, further progress is needed in the assessment of intercellular communication mechanisms, such as tunneling nanotubes, which contribute to mitochondrial transfer but are technically challenging to study in vivo. Transplantation can produce meaningful effects, at least in the short term, depending on the delivery method, dosage, and source of mitochondria. Additional manipulations may enhance mitochondrial integration, modulate immune responses, or improve targeting to the appropriate tissue. However, it remains essential to understand how transplanted mitochondria interact with a much larger population of resident ones and to characterize both the short- and long-term effects of transplantation. This knowledge will help determine which strategies are truly beneficial. Such benefits may arise from whole mitochondria, their components, or even from transient cellular responses triggered by the presence of exogenous mitochondria.
MitoWorld: What do you say to those who contend that transplantation, at best, is a reaction to the presence of transplanted mitochondria, not that transplanted mitochondria are functionally integrated into recipient cells?
Sancak: This is an important question that highlights the significance of understanding what happens at the molecular level once the external mitochondria are delivered to the recipient cells. Most animal experiments show that the transplanted mitochondria must be functional to provide a positive outcome in the recipient cells. This suggests that the recipient cells’ reaction to presence of transplanted mitochondria is not the whole story, and transplanted mitochondria function is important. I think it is more likely that both mechanisms will play a role, and depending on the disease, transplantation method, and recipient cell, one mechanism may play a more prominent role than the other.
Quintana: This is a critical question that indeed needs clarification. Are transplanted mitochondria directly restoring function, or are they instead exerting indirect effects that still benefit the recipient cell or tissue? The latter could involve activation of stress-response pathways that partially restore homeostasis. Again, the source or method to deliver mitochondria may be key to what response is engaged, and the functional integration of mitochondria may not always be necessary to explain beneficial outcomes. Depending on the kind of transfer, whole mitochondria, or at least mitochondrial DNA, may escape degradation and integrate into the acceptor cell. Even in this scenario, we still need to assess whether and how their contribution reconfigures the native mitochondrial content, and what other events may occur in parallel.
MitoWorld: What does your research from actual cases tell you about what the transplanted mitochondria are actually doing?
Sancak: The transplantation studies I was involved in were focused on safety, and no clinical outcomes other than safety were monitored rigorously. What I can say is that mitochondrial transplantation appears safe in every system tested, which makes it more appealing to pursue as a potential therapeutic intervention. We still need to systematically investigate which mitochondrial functions are the most important.
Quintana: We observe spontaneous mitochondrial transfer in the nervous system, particularly at neuron-glia connections, in both healthy tissue and in pathological contexts, such as glioblastoma. The latter represents another dimension of transfer, where cancer-neural connectivity and mitochondrial exchange are emerging as key factors in cancer progression. We see that, in physiological contexts, transfer occurs spontaneously and is regulated by specific molecular players involved in intercellular communication and dynamics. Notably, we observe that different ways of transfer or mitochondrial acquisition serve to reconfigure the mitochondrial signature and metabolism in the nervous system and glioblastomas, with the potential to modulate their physiology and offer new venues for therapeutic interventions.
Recommendation
Having been involved in this topic for some time, MitoWorld has discussed a simple step toward moving from debate to a methodology to review what is being discovered in mitochondrial transfer (endogenous) and what is being performed in mitochondrial transplantation (exogenous). Here are the suggestions and more are welcome from the community.
- Establish a working group to track developments
As Brestoff, Keshav, et al. did with nomenclature, MitoWorld suggests the establishment of an agreed-upon tracking system for transfer and transplantation activity. This could be a formal registry, an inventory, or catalog. It will include common terminology and naming of activity, methods, collection, evidence, results, conclusions, and recommendations. We are asking a number of researchers to help in this process.
- AI review of literature and associated data
MitoWorld has a relationship with Heureka Labs, developed in part by mitochondrial and metabolic researcher and AI specialist Matthew Hirschey, PhD (Duke University School of Medicine). Heureka will develop an initial approach to use AI to index past research for categories of activity and to develop data standards for analyzing and synthesizing data and processes.
- Basic science and the phenomenology of mitochondria
There is still much to learn about our endosymbionts, the mitochondria, along with their DNA, and the complex mitonuclear system. Mitochondria have suffered years of obscurity in many forms of research and medicine. They have been typecast as the powerhouse of the cell. mtDNA is just beginning to be a larger topic, with the first conference on the subject having been held this summer in Nashville, Mechanisms of Mitochondrial DNA Mutation and Repair. We would like to see the still poorly understood mechanisms of mitochondrial biology become more central to funding agencies around the world, as it is increasingly apparent that mitochondria, as the hubs of metabolism, are central to the health of our cells.
A collective effort across the mitochondrial research and clinical communities has sought to play down the “powerhouse of the cell” phrase as the sole description of mitochondria and, instead, to elevate the amazing multiplicity of mitochondrial functions. Top among those functions is mitochondrial signaling. The leaders in the signaling field will be gathering at the Keystone “Mitochondria Signaling in Physiology and Disease Symposium,” Feb 09–12, 2026, at the Keystone Resort, Keystone, Colorado in the U.S, whose keynote speaker is Anu Suomalainen Wartiovaara, University of Helsinki, presenting “Lessons Learned from Patients with Mitochondria Mutations for Physiology and Diseases.” [Conference Flyer]
Scientific organizers, Navdeep Chandel, Northwestern University Feinberg School of Medicine, and Aleksandra Trifunovic (video), Institute for Mitochondrial Diseases and Aging, University of Cologne, among the most published on the topic, have brought together a very strong group of international speakers to present findings and stimulate dialog. Among them is José Antonio (Tonio) Enríquez, Professor and Group Leader of the “Functional Genetics of the Oxidative Phosphorylation System (GENOXPHOS)” Laboratory at the Spanish National Center for Cardiovascular Research (CNIC) in Madrid, Spain.
Because of Tonio’s expertise in mitochondrial bioenergetics, oxidative phosphorylation (OXPHOS) and mitochondrial signaling and communication, MitoWorld asked him to answer a few questions about mitochondrial signaling and its significance to build the platform for understanding mitochondria more completely.
MitoWorld: What is the significance of this conference in terms of content, collaborations and the field of mitochondrial signaling?
Enríquez: This Keystone conference represents a pivotal moment in mitochondrial research, marking the formal recognition of mitochondria as central signaling hubs rather than mere energy factories. The conference, organized by Navdeep Chandel and Aleksandra Trifunovic, brings together field leaders who have fundamentally reshaped our understanding of mitochondrial biology over the past 25 years.
MitoWorld: Why is the conference important to do you individually? Can you introduce your area that relates to signaling?
Enríquez: My research area directly relates to signaling through the study of metabolic channeling and respiratory supercomplex assembly. These structures are not merely efficient ATP production units. They represent sophisticated signaling platforms that regulate ROS production, metabolite flux, and cellular stress responses. The spatial organization of respiratory complexes influences how electrons flow through the chain, affecting both energy production and generation of signaling molecules, such as superoxide and hydrogen peroxide. Furthermore, my work on aging mechanisms connects directly to mitochondrial retrograde signaling pathways that communicate cellular stress to the nucleus, triggering adaptive responses or, when dysregulated, contributing to age-related pathologies.
MitoWorld: It seems that “signaling” always must be added to any mitochondrial discussion to get beyond the APT/powerhouse conversations. Talk about how we should see mitochondria and mtDNA as part of the signaling functions in cells with the nucleus and beyond.
Enríquez: The persistent need to add “signaling” to mitochondrial discussions reflects decades of reductionist thinking that portrayed mitochondria solely as cellular powerhouses. This ATP-centric view, while historically important, has become a conceptual limitation that obscures the true complexity of mitochondrial function. Mitochondria and mtDNA function as integrated signaling networks with multiple mechanisms.
- Metabolite signaling: Mitochondria produce signaling metabolites (e.g., α-ketoglutarate, succinate, acetyl-CoA, and citrate) that directly regulate nuclear gene expression through epigenetic modifications. These metabolites serve as cofactors for chromatin-modifying enzymes, linking mitochondrial metabolism to nuclear transcriptional programs.
- ROS as signal transducers: Rather than just being toxic byproducts, mitochondrial ROS function as essential signaling molecules that activate stress-responsive pathways, regulate hypoxia responses, and control cellular fate decisions. The spatial and temporal regulation of ROS production allows mitochondria to communicate specific information about cellular energetic and redox status.
- Retrograde signaling pathways: Mitochondria communicate their functional status to the nucleus through calcium-calcineurin signaling, AMPK activation, and transcription factor regulation. These pathways allow cellular adaptation to mitochondrial dysfunction and coordinate nuclear gene expression with mitochondrial needs.
- mtDNA as an inflammatory signal: Cytoplasmic release of mitochondrial DNA activates innate immune pathways through cGAS-STING signaling, linking mitochondrial damage to inflammatory responses. This represents a fundamental immune surveillance mechanism that monitors mitochondrial integrity.
MitoWorld: List and discuss the various types of signaling and the ones you personally are interested in.
Enríquez: The diversity of mitochondrial signaling mechanisms reflects the evolutionary origin and cellular integration of these organelles.
- Metabolite-mediated signaling: This includes one-carbon metabolism products (SAM, formate), TCA cycle intermediates (α-KG, succinate, fumarate), and lipid signaling molecules (cardiolipin, ceramide). These metabolites regulate epigenetic modifications, transcriptional programs, and enzymatic activities throughout the cell.
- ROS Signaling: Different mitochondrial sites produce distinct ROS species with specific signaling functions. Complexes I and III generate superoxide with different submitochondrial localizations, affecting cytoplasmic versus matrix signaling pathways. H₂O₂ serves as a diffusible signaling molecule that modifies cysteine residues on target proteins.
- Calcium signaling: Mitochondria function as calcium buffers and signal processors, with calcium uptake and release coordinating with cellular calcium oscillations to regulate gene expression, enzyme activities, and cellular excitability.
- Mitokine secretion: Mitochondrial stress triggers the release of signaling proteins, such as FGF21, GDF15, MOTS-c, and Humanin, that act in autocrine, paracrine, and endocrine manners to coordinate tissue responses. These represent a new class of stress-responsive hormones.
- Intercellular mitochondria or mitochondrial components transfer: Direct transfer of mitochondria or mitochondrial components between cells represents a mechanism for intercellular signaling that can modify recipient cell function.
- Epigenetic regulation: Mitochondrial function directly influences nuclear chromatin structure through metabolite availability, NAD+/NADH ratios, and histone modification enzyme activities. This creates a direct link between mitochondrial metabolism and gene expression programs.
Personally, I am most interested in ROS signaling mechanisms and metabolite-mediated epigenetic regulation, as these directly relate to my research on respiratory complex assembly and aging mechanisms.
MitoWorld: If we are to re-define mitochondria how important is signaling and what might the inclusive definition include?
Enríquez: Signaling is critically important because it represents the mechanism by which mitochondria integrate their traditional functions with cellular and organismal physiology. Without signaling, mitochondria would be isolated organelles incapable of coordinating their activities with cellular needs or communicating their status to other cellular compartments. The new paradigm recognizes mitochondria as “cellular command centers” that process information, make decisions, and coordinate responses rather than simply executing metabolic programs
MitoWorld: For newcomers to the field, what would you tell them in terms of the importance of signaling in general and mitochondrial signaling in particular?
Enríquez: For students and PhD candidates entering the field, I would emphasize several key points.
- Understanding signaling as fundamental biology: Every cellular process, from development to disease, involves signaling networks. Students should approach mitochondria as integrated systems rather than isolated organelles.
- Interdisciplinary perspective is essential: Modern mitochondrial research requires integration of biochemistry, cell biology, physiology, bioinformatics, and clinical medicine. Students should develop broad competencies and collaborative skills to address complex mitochondrial questions.
- Technical diversity: The field requires expertise in diverse methodologies—from single-cell analyses and live imaging to omics approaches and animal models. Students should gain experience with multiple technical approaches to study mitochondrial function.
- Clinical relevance: Mitochondrial signaling dysfunction underlies numerous diseases, including cancer, neurodegeneration, metabolic disorders, and aging. Understanding the translational potential of basic research enhances both scientific impact and career opportunities.
Students must understand that signaling represents the mechanism by which mitochondria exert their biological effects beyond energy production. Dysregulated signaling, not simply energy deficiency, underlies most mitochondrial contributions to disease pathology.
We invite you to read our new article, “Welcome to the Mitoverse,” featured in the October 2025 issue of STEM Magazine—a widely read online publication reaching K–12 STEM teachers, college instructors, and faculty across the United States and beyond.
We’re thrilled to bring the world of mitochondria to a broader educational audience as part of www.MitoWorld.org’s mission to expand understanding of cellular dynamics, the mitochondrial genome, and the crucial mito-nuclear axis.
Why We Wrote “Welcome to the Mitoverse”
As we developed the article—written as an FAQ on MitoWorld—we realized how few straightforward, accurate, and well-referenced explanations exist for what mitochondria really are: their origins, their roles in health and disease, and their central place in modern biology and medicine.
We also recognized a deeper challenge. While genetics and the microbiome have each had their revolutions, the mitochondrial revolution is only beginning. Raising awareness must start early—in schools—where students’ natural curiosity can be fostered with accurate, up-to-date narratives about how life works.
Help Us Build a Mito-STEM Curriculum
This publication represents an opportunity to start a new effort we call MITO-STEM— partnerships connecting K–12 teachers, college instructors, and mitochondrial researchers. Our hope is to engage educators who want to introduce students to the remarkable world of mitochondria: their dynamic structure, their unique DNA, and their continuous dialogue with the nucleus and the rest of the cell.
In most biology classrooms, cells are still depicted as static spheres with a few scattered mitochondria—an image that bears little resemblance to reality. Yet understanding how mitochondria actually function, and how they dynamically coordinate and communicate with the nucleus, is essential to understanding life itself.
If you are interested in participating, please contact info@mitoworld.org
Mainstreaming Mitochondria
At MitoWorld, our mission is to mainstream mitochondria—to make their importance visible in both public understanding and medical research. Greater awareness will help drive funding for conditions ranging from rare mitochondrial diseases at birth to neurodegenerative disorders in later life.
By connecting scientists and educators through MITO-STEM, we hope to reshape how biology is taught and understood—inspiring students to see the living cell as a vibrant, interconnected system and mitochondria as its central players.
We invite teachers, researchers, and institutions to join us in this effort. Read “Welcome to the Mitoverse” in STEM Magazine’s October 2025 issue, and explore how you can get involved at www.MitoWorld.org.
www.MitoWorld.org is committed to raising public, professional and patient community awareness globally about mitochondria science, diseases, dysfunction and health. As a central resource, MitoWorld strives to share advances in mitochondrial research and clinical practice.
Guided by a senior scientific advisory board (SAB) comprising leading mitochondrial researcher and clinician-researchers and several mitochondrial medicine clinicians (Medical Advisors).
MitoWorld’s mostly volunteer Team includes three postdoc level gifted young investigators, a senior editor and writer, talented web developer and long-time patient and industry relations expert.
Together, this team with the advisory boards’ guidance produces, collects, and publishers external resources on the site and then internally produces a constant stream of high-quality original media.
- MitoBlog. We post on the latest research papers, profile mitochondrial researchers and clinicians, portray mitochondria labs globally, and report on major conferences.
- MitoCast. We conduct video interviews and accumulate information from leading researchers and clinicians.
- MitoNews. We post articles from outside sources and feature mitochondria newsfeeds from PubMed, Nature Portfolio, PRNewswire and Google on our homepage.
- Mito Events. Posting upcoming conferences and symposia and, in many cases, providing special coverage of the upcoming events through media partnerships with the conference companies and academic organizers.
- “Beyond the Disease”. In partnership with the United Mitochondrial Disease Foundation (UMDF.org), we compile a monthly set of papers to be published in their newsletter.
The core information resources on the site include a directory of leading mitochondrial researchers, academic institutions, patient organizations and clinical centers (LINK).
We are a participatory, community building nonprofit organizations. We invite inquiries, participants, and we are always looking for collaborators, supporters and funders. Feel free to reach out and help us build the “Mitochondrial Revolution” (Contact)
MitoWorld™ is a project of the California-based national R & D human capital and STEM nonprofit, National Laboratory for Education Transformation, NLET.
When Gordon Freedman, NLET’s founder and former journalist, discovered he had several mitochondrial disorders, NLET launched MitoWorld to help get the word out about the emerging potential of mitochondrial research to help across the health and disease spectrums.
Do neurons help cancer spread? In a paper published in Nature, a multi-institution research team, led by Simon Grelet at the University of South Alabama, provides strong evidence for a key relationship between cancer cells and neurons. They showed that mitochondria migrate from neurons to cancer cells to increase the metabolism of the cancer cells.
Dr. Grelet’s team focused on the mitochondria in cancer cells. The spread of tumors requires a significant amount of energy, and mitochondria produce energy for the cells. Cancer cells are well-known for adapting their metabolism to fit changing conditions. However, this metabolic plasticity was thought to be due to changes within the tumor cells themselves. For example, they could obtain energy by glycolysis (a less efficient process for producing ATP in the cytoplasm) or by oxidative phosphorylation (a more efficient process in the mitochondria). However, cancer cells also receive outside help in the form of metabolites, growth factors and cytokines from other cells.
Previous experiments had shown that somehow the neurons aid tumor progress, but what really interested the Grelet team was a relatively new concept that mitochondria can move from cell to cell. When neurons were co-cultured with tumor cells, the neurons experience changes to their metabolism. The number of their mitochondria increases, and some are transferred to the tumor cells. How could this work?
The team first looked at a co-culture of an aggressive breast cancer cells and neurons. The neurons underwent a morphological change from globular to tubular structures, which indicated the cancer-induced differentiation of the neurons. Neuronal differentiation is associated with changes of metabolic programming from glycolysis to oxidative phosphorylation. These changes were also associated with the establishment of long neuron protrusions, forming a neural network in the culture in vitro, which reflects the establishment of a nerve-cancer crosstalk and suggests the communication or sharing of biological materials.
Next, the team used fluorescent-labeled mitochondria to show that the mitochondria migrated from neurons to cancer cells. These methods revealed additional insights into the transfers, but they had significant limitations. To overcome those limitations, the team developed MitoTRACER. This system used genetic engineering where the donor cell mitochondria carry a tag protein that, once transferred to the recipient cells, triggers an enzymatic reaction activating the permanent expression of a fluorescent protein. The trick is that, when mitochondria move from the neurons to the cancer cells, the red fluorescence is lost, and a green signal is permanently activated. Thus, it is easy to monitor cells with mitochondria that have migrated into a new cell.
Using this unique approach, the researchers have been able to investigate the fate of the recipient cells during the cancer progression cascade, and by fate mapping of the recipient cells from the primary tumor during metastasis progression in vivo. The researchers noted enrichment of acquired mitochondria in brain metastases that might indicate enhanced metabolic plasticity from those extra mitochondria. Neuronal mitochondria are more metabolically active and might better enable tumor cells to thrive in the brain environment. This approach allowed us to define the role of mitochondrial transfer in the primary tumor environment. This process generates a subset of highly efficient metastasis cells that succeed through the complex stops and that are resilient to the metastatic barriers to ultimately form distant metastases, which is the main driver of cancer-associated mortality.
In summary, this fascinating paper might have significant implications for future cancer therapies, and beyond the cancer context, the mitoTRACER approach could have broader applications in studying cell-cell transfer of mitochondria in health and disease to understand the physiopathological implications of these transfers better.
Discussion with Dr. Grelet
MitoWorld: Your paper brings to mind the work of Judah Folkman who showed that tumors need and encourage the formation of a blood supply to progress. What do you believe the tumor may be getting from the nerve cells?
Interesting comparison. Yes, there are definitely commonalities between cancer angiogenesis and cancer innervation. In fact, cancer can actively “call” neurons to innervate them. In the context of cancer, we recently showed that aggressive subtypes of breast cancer cells can secrete axon guidance molecules, including Semaphorin-4F, to promote cancer innervation. We also found that this increased nerve density is associated with enhanced metastasis (PMID: 34810279).
The role of axon guidance molecules in promoting cancer innervation was demonstrated years ago by Dr. Gustavo Ayala (PMID: 11746267; PMID: 24097862), who pioneered the field of cancer innervation and collaborated with us on this study. Since then, many studies, including our own, have confirmed the contribution of these molecules to cancer innervation and cancer aggressiveness. While increased nerve density is often associated with poor clinical outcomes, the underlying mechanisms have remained poorly understood. This gap in understanding is precisely what motivated us to conduct this study.
MitoWorld: The movement of mitochondria from cell to cell is still controversial. What do you think it will take to solidify the concept?
The idea of intercellular mitochondrial transfer remains controversial, largely due to the lack of robust tools and clear in vivo evidence. To solidify the concept, new rigorous and physiologically relevant approaches are needed. For example, genetic systems, such as our MitoTRACER approach, which allow for precise and conditional signaling of transfer events, open the avenue for lineage-based tracking of transferred cells in vivo. Such models are critical to move the field forward and to convincingly demonstrate that mitochondrial transfer is not merely an artifact, but a biologically meaningful process.
MitoWorld: How do you think the cells signal to each other to initiate the transfer of mitochondria?
A variety of signals could potentially be involved in initiating mitochondrial transfer, but these remain to be better defined. In the context of cancer innervation, axon guidance molecules may contribute; more generally, transfer events may occur as part of a stress or help response, or by hijacking existing physiological communication routes. These signals could include reactive oxygen species, cytokines, or changes in membrane potential or lipid composition. Cancer cells, for instance, can upregulate molecules involved in cell-cell contact to facilitate mitochondrial transfer, as elegantly demonstrated by Watson et al. (PMID: 37169842). Deciphering the molecular language of this intercellular request remains a critical next step for the field.
MitoWorld: These experiments seem to have ramifications for how the nuclear and mitochondrial genomes coordinate their activities. Do you think the communication between the donated mitochondria and the recipient cell also involves the donor genes?
Absolutely, and this is a topic that warrants further investigation. Mitochondrial transfer introduces not only a new metabolic organelle with all its associated machinery, but also foreign mitochondrial DNA into the recipient cell, raising important questions about nuclear–mitochondrial coordination. While the nuclear genome of the recipient cell continues to govern most mitochondrial functions, the donor mitochondria carry their own genome and organelle machinery, which in our case is fine-tuned for neuronal metabolism and may not be fully compatible. This mismatch could influence mitochondrial gene expression, protein stoichiometry, and ultimately, the bioenergetic output. Whether donor mitochondrial DNA or its transcripts actively modulate recipient cell behavior remains an open and fascinating question. Clarifying the extent and mechanisms of this intergenomic crosstalk is essential to fully understand the consequences of mitochondrial transfer.
MitoWorld: You note that more work is needed to determine if the effects of the donated mitochondria are related to metabolic efficiency or simply that there are more of them. Do you have any sense of which it might be?
In the context of neurons, it is likely a combination of both abundance and quality. On one hand, the increase in mitochondrial mass may help support basic energy demands, particularly under stress. On the other hand, the quality and origin of the donated mitochondria, such as their neuronal bioenergetic efficiency, may actively contribute to metabolic reprogramming in the recipient cell. In our system, the integration of neuronal mitochondria appears to enhance not only energy production but also metabolic plasticity, enabling cancer cells to better adapt to new microenvironments. Dissecting the relative roles of mitochondrial abundance versus functional impact will be key to understanding how mitochondrial transfer influences cell fate and behavior.
MitoWorld: Folkman used his findings to suggest that cancers could be treated by preventing angiogenesis, and that is now widely accepted. Do you have any thoughts on how your findings with neurons might be used to develop therapeutic strategies for cancer?
Yes, absolutely, that is the ultimate goal. There are several possible strategies. First, we can target tumor innervation itself, which supports cancer progression. Second, we can aim to block the intercellular transfer of mitochondria, which fuels cancer cell adaptation. Third, and perhaps most compelling, we can selectively target recipient cancer cells that have acquired unique metabolic or phenotypic traits as a result of mitochondrial uptake. These cells may represent a vulnerable subpopulation that could be eliminated through precision therapies. Together, these approaches offer a new framework for tackling cancer’s adaptability.
MitoWorld: You looked at breast cancer and melanoma cells, both highly metastatic cancer types. Is the neuronal connection equally valid in less metastatic cancers?
We also previously reported a link between cancer plasticity and cancer innervation (PMID:37046688). Our findings suggest that more aggressive cancer cells are more likely to establish neuronal connections and engage in mitochondrial transfers. This, in turn, may further amplify their aggressive behavior, creating a vicious cycle. The ability of these cells to co-opt neural signaling and reshape their metabolic and phenotypic programs reflects a high degree of plasticity that likely contributes to disease progression.
MitoWorld: Also your work focused on solid tumors. Is there anything to be learned about blood tumors?
Interesting point. Blood cancers reside in richly innervated niches, such as the bone marrow, where neurons regulate hematopoiesis and immune responses. So, similar mechanisms might shape the behavior of leukemia or lymphoma cells. However, this remains largely unexplored, and adapting lineage-tracing tools, such as MitoTRACER, to hematological models could open exciting new directions in the field.
Reference
Hoover G, Gilbert S, Curley O, Obellianne C, Lin MT, Hixson W, Pierce TW, Andrews JF, Alexeyev MF. Ding Y, Bu P, Behbod F, Medina D, Chang JT, Ayala G, Grelet S (2025) Nerve-to-cancer transfer of mitochondria during cancer metastasis. Nature
Dr. José Antonio Enríquez—known to his lab simply as Toño—leads the Functional Genetics of the Oxidative Phosphorylation System (GenOXPHOS) group at the Spanish National Centre for Cardiovascular Research (CNIC). Using large-scale bioinformatics, his lab investigates many aspects of mitochondria, including how their protein complexes assemble, the pathophysiology of mitochondrial diseases, and even the evolutionary history of mitochondrial proteins.
Toño’s path to mitochondrial science began at the University of Zaragoza, where he completed his PhD. He then moved to California for a postdoc at Caltech before returning to Zaragoza to establish his first lab as a Principal Investigator. About 15 years ago, he moved his lab to CNIC, where he continues to push the boundaries of mitochondrial biology.
When asked what drew him to this field, Toño recalled:
“When I finished my biology degree, I knew I wanted to dedicate my life to science, but my interests were broad. I wasn’t drawn to one specific topic or focused on curing a particular disease. I was more interested in understanding the logical rules behind life itself. During a lab rotation at the University of Zaragoza, I encountered mitochondrial DNA (mtDNA). I was fascinated by the fact that this tiny but essential chromosome lives outside the cell nucleus. The idea of an ‘outsider’ chromosome inside a eukaryotic cell sparked my curiosity, and that’s what brought me to mitochondrial research.”
Known for his passionate and fiercely curious nature, Toño fosters a lab culture that encourages creativity, independence, and open scientific debate. He pushes his lab members to think outside the box—not just in their experiments, but in how they approach problems, question assumptions, and imagine what might be possible. He thrives on “crazy” ideas and welcomes disagreement as a sign of engaged thinking. Weekly lab meetings often begin with him sharing a new paper, a philosophical question, or a hypothesis that came to him out of the blue.
What are the big questions ahead for mitochondrial research?
“Mitochondria continue to surprise us,” says Toño. “From their own unique DNA and divergent genetic code to their roles in apoptosis, signaling, and disease, there’s always something unexpected. The OxPhos system alone is remarkably complex in both structure and function.”
As for what’s coming next?
“I think the most important discoveries may still be ones we don’t expect. But if I had to name specific questions for the coming year, I’d point to three:
- Understanding how sodium (Na⁺) helps build the mitochondrial membrane potential,
- Figuring out how cells maintain different types of specialized mitochondria within a single cytoplasm, and
- Resolving the debate over whether mitochondria can move between cells in a physiologically meaningful way.”
A major breakthrough: SCAF1 and mitochondrial supercomplexes
One of the lab’s most exciting discoveries was identifying the protein SCAF1 (supercomplex assembly factor 1), which enables the physical interaction between two key components of the electron transport chain—complex III and complex IV.
“This was a big step in supporting our ‘plasticity model’ of how the mitochondrial electron transport chain is organized,” says Dr. Enríquez. “We were also excited to show that variations in mtDNA can influence metabolism and healthy aging. And our recent finding that respiration complex I acts as a sodium/hydrogen (Na⁺/H⁺) antiporter revealed that sodium plays a major role in building the mitochondrial membrane potential.”
Meet the GenOXPHOS Team:
The GenOXPHOS lab currently includes around 10 members, each pursuing their own research, but generally, the group can be divided into the following research directions.
Mitochondrial Supercomplexes and Their Role in Health
This team includes three graduate students, each using different strategies to understand how respiratory supercomplexes are assembled and what role they play in health and disease.
Carmen Morales Vidal studies a highly conserved supercomplex made up of respiratory complexes I and III, exploring the importance of this interaction in mammalian cells.
Paula Fernández-Montes Díaz focuses on a family of complex IV protein isoforms, each of which is responsible for a different conformation of complex IV. These variants allow tissues to fine-tune their metabolism based on specific energy needs.
Sara Natalia Jaroszewicz specializes in advanced super-resolution microscopy to visualize these supercomplexes inside intact cells. Until recently, this was only possible using indirect and often disruptive methods.
Heart-Specific Mitochondria
Located in a cardiovascular research center, the lab has a strong focus on heart-specific mitochondrial biology.
Dr. Michaela Veliova, a postdoctoral researcher, studies different subtypes of mitochondria within individual heart cells. She’s investigating how these subtypes form and function and what roles they play in disease.
Dr. Rebeca Acín, a senior scientist, examines the reversal of ATP synthesis, a process where ATP synthase (normally making ATP) starts breaking it down. While this may help with mitochondrial quality control, Rebeca is exploring its connection to disease. She’s also investigating how ATP synthase dimerization (its ability to form pairs) affects this reversal process.
Translational Research: From Discovery to Therapy
This part of the lab focuses on translating basic mitochondrial science into potential therapies.
Dr. Marta Pérez-Hernández Durán, a postdoctoral researcher, is studying a protein kinase called FGR that regulates the activity of mitochondrial complex II. Stress-dependent activation of FGR increases reactive oxygen species (ROS) production and stabilizes HIF1a, ultimately leading to increased release of inflammatory cytokines. Since inflammation is present in numerous heart diseases, Marta is testing whether blocking FGR could be a promising treatment.
Dr. Rebeca Acín is exploring another potential drug target. OMA1, a stress-activated mitochondrial protease can trigger fragmentation of mitochondria. She is examining whether modulating its activity could help prevent mitochondrial damage in disease.
Bioinformatics and Structural Modeling
This line of research seeks to uncover how mitochondrial structures and genetic interactions shape function and dysfunction.
Dr. Jose Luis Cabrera Alarcón, a postdoctoral researcher, studies evolutionary conservation of mitochondrial genes at the population level, with the aim of identifying how genetic incompatibilities between nuclear and mitochondrial genomes might contribute to disease.
Marina Rosa Moreno, a graduate student co-mentored by Dr. Enriquez and José Luis, studies the structural biology of respiratory chain complexes. Using computational modelling and cryo-electron microscopy, she investigates how the respiratory chain complexes assemble and how structural variations may affect energy production and pathology.
The Lab’s Backbone
A great research environment doesn’t just depend on bold ideas. It also relies on the people who keep things running. GenOXPHOS is supported by a dedicated technical team:
Dr. María Concepción Jiménez Gómez, the lab manager, keeps operations smooth and organized.
Eva Raquel Martínez brings deep expertise in histology and molecular biology techniques.
Dr. Raquel Martínez de Mena oversees tissue culture and cell maintenance.
María del Mar Muñoz Hernández, the lab’s mouse technician, specializes in advanced animal procedures critical for the in vivo and translational work.
If our website is MitoWorld, the Mechanisms of Mitochondrial DNA Mutation and Repair conference was the introductory gathering of what could be called “mtDNA World.”
The organizers, Patrick Chinnery (Cambridge), Agnel Sfeir (Sloan Kettering) and Michal Minczuk (Cambridge), emphasized that this conference focused solely on mtDNA is a first of its kind.
“This brand-new conference will focus on understanding how mitochondrial DNA mutations occur in the germ line and somatic tissues with age and how they contribute to common diseases, including neurodegeneration and cancer. The conference will also cover mitochondrial DNA’s molecular and cellular consequences and new approaches to repair and remove mutations.” [conference website]
The global mitochondria conference circuit generally is focused on mitochondria themselves (often in primary mitochondrial disease) in all their complexity with a smaller percentage of presentations on mtDNA itself. In Nashville, June 1–5, about 75 individuals representing labs globally, went deep into a range of heteroplasmy dynamics over lifetimes and in various disease and dysfunction cases. There was a sense of the importance of mtDNA and its relationship with the nuclear DNA as a primary and secondary driver of disease and dysfunction and also as part of the fundamental aging process.
“The result was an interactive meeting that highlighted the current multi-functional nature of mtDNA (beyond its known role in ATP production) and the cutting-edge new techniques and approaches now available to understand how mtDNA genes are expressed, how mtDNA mutations contribute to human physiology and pathology, and how we can now edit mtDNA or otherwise modulate this maternally inherited genome to improve human health,” said Gerry Shadel (Salk Institute).
The conference was very participatory and, since it was held in Nashville, ended with an evening of line dancing.
In the words of some of the organizers and attendees:
Agnel Sfeir, Organizer, Sloan Kettering
The meeting exceeded our expectations in every way. The quality of the science, the level of engagement, and the sense of community were truly exceptional. One of our goals was to create a space that fostered open discussion across disciplines and career stages, and I think we succeeded, which was evident by the engagement of trainees, the quality of their presentations, and the insightful questions they asked.
Dmitry Temiakov, Thomas Jefferson University
The conference’s exclusive focus on mitochondrial DNA was both timely and highly valuable for the scientific community. By concentrating on mtDNA, the meeting brought together researchers across diverse disciplines—from genetics and structural biology to clinical medicine—who might otherwise not engage in direct dialogue. This focused format fostered in-depth discussions on unresolved questions, including the mechanisms underlying mitochondrial diseases, maternal inheritance, and the role of mtDNA in inflammation and aging.
Maria Falkenberg, The Falkenberg Lab, University of Gothenburg
The meeting was a unique and refreshing experience, being the first to focus only on mtDNA. It gave space for interesting discussions that went all the way from basic science to possible new treatments. The talks covered many parts of mtDNA biology, from how it is maintained to how it can be targeted in disease. It was great to see the community come together around a topic that is often included in bigger meetings, but not usually the main focus.
Gerald Shadel, Salk Institute
Our genome comprises nuclear and mitochondrial DNA, both of which are essential for life and contribute to human diseases and aging. The biology and genetics of mtDNA is complex due to it being present in multiple (often thousands) copies/cell and its sequence dynamically changing in our bodies as we age. While there are many meetings on nucleic acids (DNA and RNA), genetics and even mitochondria, rarely is mtDNA a central theme. This FASEB meeting was therefore unique by focusing a lens on mtDNA and effectively bringing together many of the senior researchers who have long influenced our understanding of mtDNA with exciting new investigators in the field.
Carlos T. Moraes, University of Miami
It was right time for a meeting focused on my favorite genome (mtDNA). There have been so many advances in our understanding and manipulation of mtDNA in the last few years, and it was exhilarating to hear and discuss them with experts and colleagues. My recent area of work is mtDNA editing, and new techniques have opened a whole area of investigations and therapeutic development. As always, new knowledge raises many questions, so this meeting was a great forum to generate new ideas and how to overcome barriers, such as the off-target edits of mtDNA base editing.
Amutha Boominathan, MitoSENS
The conference provided a comprehensive overview of recent advances in mitochondrial DNA research, with a strong focus on its role in cellular function and pathology. A key highlight was the application of advanced sequencing technologies to resolve mitochondrial heteroplasmy at the single-cell level and to establish genotype-phenotype correlations. It brought together students and junior and established researchers, with particular emphasis on emerging topics, such as mitochondrial regulation of immune responses, novel metabolic functions, and targeted approaches to silence/modulate the mitochondrial genome. The meeting was highly interactive and engaging. Looking forward to the follow-up!
Olvia Conway, Duke University
This meeting was extremely valuable to me as a trainee because of the networking and learning opportunities available. My mtDNA project is a new area for the lab, so this meeting was a way to meet others focused on this topic, receive feedback on some of my early work, and determine in which direction the field is heading. I am grateful for the opportunity to talk to other scientists during the conference sessions, and I am planning on implementing many of the suggestions I received. This was my first meeting as a graduate student, and I had a great experience.
Ana Andreazza, PhD, professor of pharmacology and toxicology at the University of Toronto’s Temerty Faculty of Medicine, leads the Mitochondrial Innovation Initiative, Mito2i, a research hub at University and affiliated institutions and hospitals.
The new project, MitoRevolution: Mitochondrial Transplantation Transforming Regenerative Medicine — from research to patient care to global impact, is part of the university’s
Institutional Strategic Initiative portfolio, is supported by a $23.8-million grant from the Canadian federal government’s New Frontiers in Research Fund Transformation Stream and brings together an interdisciplinary team that is committed to transforming regenerative medicine through mitochondrial transplantation.
Mitochondrial transplantation is defined as the process of introducing new mitochondria into cells, tissues or organs, and mitochondrial transfer is the natural movement of mitochondria between cells or into bodily fluids.
These processes are both controversial, and mitochondrial transplantation as a therapy is viewed with a considerable skepticism. Nevertheless, there is a growing interest in research into transplantation for emergency, resuscitation and regenerative purposes. Some cases have yielded positive results. However, those results cannot be attributed to an increase in mitochondrial capacity and function or to actions by the immune system or other reactions.
The infusion of federal funding in Canada to explore the wide-ranging question posed by mitochondrial transplantation marks the first nationally funded initiative of its kind.
Discussion with Dr. Andreazza
MitoWorld: There seems to be a real divergence in the thinking in the scientific community of whether transplantation is real in terms of transplanted mitochondria taking up their full functions once transplanted. How do you and the team answer those questions?
Andreazza: Indeed, this divergence is a major reason our team has come together under the NFRF-Transformation grant. Rather than assuming one mechanism over another, our approach is to systematically evaluate how transplanted mitochondria interact with host cells, whether by integrating functionally, or by initiating signaling pathways that support recovery or regeneration. Using innovative tools such as live imaging, mitochondrial tagging, and 3D tissue models, we aim to directly observe and measure mitochondrial behavior post-transplantation.
MitoWorld: On the other hand, there is the fear that the patient communities, especially those who have mitochondrial genetic diseases or are parents of children who do, will have their hopes falsely raised in the short term. How do you and your team counsel the mitochondrial patient community at this point?
Andreazza: We are deeply aware of the responsibility we have to the patient community. Transparency is central to our approach. While mitochondrial transplantation holds promise, we are careful not to frame it as a near-term therapeutic option for genetic mitochondrial diseases. Instead, we emphasize that this is an early-stage scientific endeavor with an initial potential for ex-vivo organ regeneration. We engage with patient groups regularly. In fact, the MitoCanada Foundation was part of the design of the project from the beginning, and it is now forming patient and communities committee that will oversee the project development. Most importantly, listening to concerns and co-developing knowledge translation strategies are central to ensure expectations remain grounded in the realities of where the science currently stands.
MitoWorld: Where do you and the cross-disciplinary and cross-institutional team hope to focus first, and what solutions or findings do you anticipate?
Andreazza: Our first focus is to establish the mechanism that underlies mitochondrial transplantation. Using 3D tissue and animal models, we hope to determine how mitochondria survive transfer, how long they persist in recipient cells, what cells uptake mitochondria, and what outcomes they influence. We’re particularly interested in ex-vivo organ regeneration for improvement of organ transplant. From this foundational science, we hope to develop tools that can guide future clinical applications, including standardized protocols and safety metrics.
MitoWorld: It would seem that Canada is the first national government to make an investment in mitochondria transplantation. What do you think motivated decision from a policy, scientific, and treatment perspective?
Andreazza: Canada’s investment reflects the country’s forward-looking research framework that embraces high-risk, high-reward strategies. It aims to elucidate the roles of mitochondria in health and in nearly every major disease with an opportunity to transform our understanding, and hopefully treatment strategies. In my view, these opportunities made this a compelling story for support under the NFRF’s Transformation Stream. Additionally, the interdisciplinary and community-driven nature of the project aligns well with Canada’s emphasis on collaboration and innovation.
The UMDF Mitochondrial Medicine for Scientists and Clinicians Mitochondrial Medicine 2025 conference provides an international stage for leaders in mitochondrial medicine and offers programs to inspire the next generation of researchers. Attendees will learn about the latest developments in the field of mitochondrial medicine, including industry advancements, potential treatments, therapies and cutting-edge research. The event also gives the scientific communities the unique experience of engaging with affected patients to better understand symptoms and work faster towards a cure. This year’s conference is being held in St. Louis, Missouri on June 18-21, 2025. https://www.umdfconference.org/
Jonathan Brestoff, MD, PhD, MPH, leads the Brestoff Lab and is Associate Professor of Pathology & Immunology, Director of the Initiative for Immunometabolism, and Medical Director in the BJH Clinical Flow Cytometry Lab at WashU Medicine in St. Louis.
We asked Jon to explain a bit about this his work and what is being organized from the scientific and medical community at UMDF 2025.
MitoWorld: Jon, how did you become involved with the UMDF Clinical & Scientific Program?
Brestoff: My lab has been working on trying to develop mitochondria transplantation as a new therapy for primary mitochondrial diseases, and this work has gotten me engaged with the UMDF. With the meeting being in St. Louis, they sought a local presence on the organizing committee. I’m very honored to help with this meeting and think it will be very exciting!
MitoWorld: What can researchers and clinicians expect from this year’s program?
Brestoff: This conference includes an amazing lineup of speakers on diverse scientific topics on mitochondrial biology and clinical issues in mitochondrial medicine. Main scientific sessions include Inflammation and Metabolic Diseases, Mitochondria on the Move, Mechanisms of Clearing Damaged Mitochondria, and Multi-omics. Clinical sessions include the NAMDAC Registry Session, Mitochondrial Medicine Society Platform, and Clinical Trial Updates. On Saturday, there are 2 parallel Master Classes, one on emerging clinical topics chaired by Dr. Michio Hirano and one on scientific career development chaired by me.
MitoWorld: Is there any particular theme or emphasis this year?
Brestoff: The main themes are around emerging scientific discoveries about mitochondria and clinical updates. One of the most exciting aspects of this meeting is that patients, families, clinicians, and scientists all come together for one conference. This creates a unique experience that, in my experience, has been incredibly motivating and inspiring.
MitoWorld: With your lab at Washington University in St. Louis, will you be discussing or your lab members presenting on your lab’s work?
Brestoff: Yes! While I am not speaking to yield time to other investigators, a couple exceptionally talented scientists from my group are presenting their work on mitochondria transfer and transplantation.
MitoWorld: What are your hopes in your work for the next year and what issues are on the forefront that may materialize over the next year?
Brestoff: There are so many new and exciting discoveries about mitochondria — how they work, what they do, and how we can leverage their biology to develop new therapeutics. There is tremendous untapped potential in this field for many diseases, not just primary mitochondrial diseases but also others like obesity, heart disease, and even aging. I hope we can find ways to team up with each other, industry partners, and investors to make some of these new therapeutics a reality for patients who need them. For my own lab, we’re currently working to make mitochondria transplantation a future possibility for patients with primary mitochondrial diseases. I hope we can get there.
The special issue of Journal of Cell Science (JCS) on the “Cell Biology of Mitochondria” looks to be one of the most comprehensive open series of papers, opinions, perspectives, interviews, reviews and posters on the subject of mitochondria biology, perhaps ever.
This incredibly in-depth examination of mitochondria covers the subject in research, interviews and commentary and does so in what can only be described as a community spirit from the Journal of Cell Science (JCS) a publication of the Company of Biologists, which is “dedicated to supporting and inspiring the biological community.”
A Good Place to Start [Editorial]
The Cell Biology of Mitochondria Special Issue is a collaboration led by Ana J. Garcia-Saez, Max Planck Institute of Biophysics and Heidi McBride, Department of Neurology and Neurosurgery McGill University, guided by Cell Biology Executive Editor Seema Grewal, who has a deep publishing and research biology background. McBride is also a member of the MitoWorld Scientific Advisory Board (SAB).
MitoWorld was so impressed with this collection, enough reading for a month, that the questions arose of how does such an issue come together and how does it stand to help the mitochondrial research world as the subject becomes more popular. To get a sense of this, Executive Editor Seema Grewal answered a few questions.
MitoWorld: What prompted the special issue?
Grewal: JCS has a long and rich history of publishing papers in the field of mitochondrial cell biology; indeed, some of the early papers examining the factors that contribute to mitochondrial fusion and fission were published in JCS. We wanted to remind the community about this, so what better way to do this than to coordinate a special issue on the topic.
MitoWorld: This was a huge undertaking, how did this get going and how long has it taken?
Grewal: We started discussing the idea at the journal’s annual gathering of editors back in February 2024. Heidi and Ana are on the journal’s Editorial Advisory Board and are experts in the field, so the team felt that they would be well-placed to serve as Guest Editors for the issue. After some discussion with them, we decided on the aim, scope and timeline for the special issue. We put out a call for papers in the Spring of 2024 and had an encouraging response from the community, resulting in lots of research articles being submitted for consideration in the special issue. In parallel, we also identified and invited experts from across the field to contribute review-type articles.
MitoWorld: Can you talk about the Journal and its mission and how you are able to put together projects at this scale.
Grewal: JCS prides itself in being a community journal that is published by a not-for-profit publisher (The Company of Biologists) that exists to benefit scientists not shareholders. Coordinating a special issue is hard work, but we’re fortunate to have an in-house team that can support Guest Editors in coordinating the issue, so that they can focus on the science. This team works closely with the Guest Editors to ensure the smooth and efficient handling of articles.
MitoWorld: What do you hope comes from such a publication? Who should be reading this issue?
Grewal: We’re hoping that the issue will inspire the community and stimulate debate and discussion. It contains a range of research and technical articles that showcase the advances in the field. It also contains some in-depth reviews that synthesize the latest findings. We’ve also included some perspective and opinion articles that challenge our view of mitochondria. Finally, we strongly believe that it’s important to highlight the scientists that actually do the work, so the issue includes some interviews with researchers at different career stages. We’re hoping there’s something in the issue for everyone. It’s also worth pointing out that, thanks to our ‘Forest of Biologists’ initiative, we planted 24 trees to represent the 24 peer-reviewed articles published in the issue, so that’s another really positive outcome!
MitoWorld: There is so much material, do you have suggestions on what busy people should concentrate on or how to best use the whole resource.
Grewal: The Opinion piece is a good place to start, as it provides an over-arching view of mitochondria. After that, we suggest that people just bookmark the full table of contents and dip in and out of any reviews or research articles that appeal to them
MitoWorld: What do you hope the take-aways are for the serious reader of this special issue?
Grewal: That we’ve made lots of progress, largely thanks to new technologies…but there’s still so much to learn!