Led by Kathryn Cullen, a research team at the University of Minnesota, the University of Queensland, and the Mayo Clinic studied depression and fatigue in young adults with and without early-stage depression. They found a positive correlation between ATP levels and levels of depression in young adults that correlates with depression and suggests a compensatory mechanism early in the disease. Their findings were published in a recent paper in Translational Psychiatry.
Fatigue is a common feature of major depressive disorder (MDD). The Cullen team wanted to better understand the origins of that fatigue to improve the quality of life of young MDD patients. To accomplish that, they compared ATP levels in cells from MDD patients and healthy controls. ATP levels were measured in brain cells by magnetic resonance spectroscopy and in peripheral blood mononuclear cells with a Seahorse instrument.
They found that the MDD patients had higher levels of ATP production than the controls, and those levels correlated positively with the measures of fatigue. In addition, those
This study is the first to show higher levels of ATP in brains and blood of MDD patients. The
findings suggest a compensatory mechanism early in the disease and may suggest strategies for future therapies.
A Conversation with Drs. Cullen and Tye
MitoWorld: Your discovery of a biosignature for fatigue in depressed youth is exciting. Can you give us an idea of where your research is going next? For example, do you plan to expand the sample size or to control for various drug treatments?
Cullen & Tye: Yes, we are actively seeking funding for this important work. Our hope is to confirm the findings from our paper in a larger group of young people. Controlling for medication can be a challenge due to ethical constraints, but it becomes more feasible with a large sample, to allow us to look at subgroups.
MitoWorld: The depression connection noted between your results and those for early Parkinson’s disease patients is interesting. It is reminiscent of the connection between early brain injury and Alzheimer’s disease. Do you have any thoughts on that?
Cullen & Tye: Given that depression is already an established risk factor for Alzheimer’s disease, we speculate that the bioenergetic signature we find could possibly represent a precursor reflecting physiological risk for dementia. If so, this biosignature could be a critical mechanistic link between the two conditions.
MitoWorld: Another recent paper showed a connection between mitochondrial health and depression. Could this be a common phenomenon? Do you think your findings would apply to muscle tissues?
Cullen & Tye: We suspect that impaired mitochondrial efficiency and capacity is likely to be reflected across all tissues. We are interested in the immune system as it is also closely linked to depression, as a mechanistic risk factor. The findings summarized in this review paper on mitochondrial health and inflammation in skeletal muscle hold potential relevance to depression, since the fatigue and low motivation in depression often contributes to sedentary behavior and muscle disuse. Taken together, an examination of mitochondrial health in muscle tissues in individuals with depression may be warranted.
MitoWorld: One of the mysteries that intrigue us is the “shared governance” of the mitochondrial and nuclear genomes. Do you have any speculation on how the nucleus signals to the mitochondria to increase the ATP levels in depression?
Cullen & Tye: This is a great question. The nucleus regulates mitochondrial ATP production indirectly through coordinated energy-sensing and transcriptional pathways, particularly via AMPK and PGC-1α, as well as rapid calcium and redox signaling that tune mitochondrial efficiency and capacity in real time. In depression, we speculate that this shared governance becomes dysregulated by chronic stress and immunometabolic adaptations to ongoing inflammatory load, resulting in the impairment of mitochondrial ATP production capacity to meet cellular demand.
MitoWorld: Do you think that your results might lead to clinical applications? For example, might the results from your MRI or PBMC studies might translate to a clinical test?
Cullen & Tye: Yes. While we are currently still in the foundational research stage, we strongly further stages of this research will have the potential to guide personalize clinical care. Part of the next steps include translating these findings to the clinic through biomarker-driven, companion diagnostic approaches.
Reference
Cullen KR, Tye SJ, Klimes-Dougan B, Wiesner HM, Varela RB, Morath B, Zhang L, Chen W, Zhu XH (2026) ATP bioenergetics and fatigue in young adults with and without major depression. Translational Psychiatry https://doi.org/10.1038/s41398-026-03904-y.
Now On-Demand: Keystone Symposia’s Mitochondria Signaling in Physiology and Disease
If you missed the Keystone Symposia conference Mitochondria Signaling in Physiology and Disease—held February 9–12, 2026 at Keystone Resort in Colorado—you now have a second chance. On Demand registration is open, giving you access to the full main-session program from one of the most significant gatherings in mitochondrial biology in recent years. See: keystonesymposia.org/conferences/conference-listing/meeting/onpage-program/b12026.
What the Meeting Was About
Co-organized by Navdeep S. Chandel, Ph.D. (Northwestern University), and Aleksandra Trifunovic, Ph.D. (University of Cologne), the symposium brought together basic scientists, clinicians, and industry researchers around a single ambitious premise: that mitochondria are not simply the cell’s power generators, but dynamic signaling hubs that coordinate metabolism, stress responses, redox biology, proteostasis, and immune activation across virtually every tissue in the body.
In Their Own Words
Dr. Chandel reflected on what the symposium set out to accomplish and what it achieved:
“The objective was to convene a cross-disciplinary community of basic scientists, clinicians, and industry researchers to redefine mitochondria not merely as bioenergetic organelles, but as dynamic signaling hubs that coordinate metabolism, stress responses, redox biology, proteostasis, and immune activation across tissues. By all measures, the meeting achieved these aims. Sessions were intellectually rigorous and highly interactive, trainees were prominently featured through talks and poster sessions, and discussions frequently extended beyond scheduled programming. Many attendees remarked on the collaborative atmosphere and the breadth of disciplines represented, reflecting a field that is both expanding and increasingly integrated.”
Maulik Patel, Ph.D., Associate Professor, Metabolism and Nutritional Programming, Van Andel Institute, offers succinct summary of the Symposium, underscoring the objectives of the gathering.
“It had been some time since I last attended a mitochondrial meeting, so the Keystone Symposium on Mitochondrial Signaling in Physiology and Disease provided a valuable snapshot of where the field now stands. While the idea of mitochondria as signaling hubs is not new, what was striking is how pervasive and mechanistically defined these roles have become—spanning metabolism, immunity, proteostasis, and aging.
The level of technical sophistication was particularly impressive: researchers can now trace signaling events from a mitochondrial metabolite all the way to specific molecular targets, sometimes down to single-residue modifications, making the conclusions far more rigorous and convincing. The meeting also showcased the extraordinary range of scales at which mitochondria are studied, from atomic-resolution structural work to whole-organism physiology, underscoring just how integrative and exciting mitochondrial biology has become.”
Janine H. Santos, Ph.D., Group Leader, National Institute of Environmental Health Sciences (NIEHS), underscores bridging basic science with translational and clinical work.
The Keystone Symposia meeting “Mitochondria Signaling in Physiology and Disease” stands out for its forward-looking reframing of mitochondria as dynamic, cell-type–specific signaling hubs that actively shape cell fate, adaptation, and disease. This perspective places mitochondrial biology at the center of physiology and pathophysiology, including in aging. The program is especially compelling for its integration of diverse areas of mitochondrial research such as metabolite, mtDNA, and redox signaling alongside stress adaptation and emerging technologies. By bridging basic science with translational and clinical insights, it highlights shared mechanisms and therapeutic opportunities across diseases. Its highly interactive format further fosters learning, cross-disciplinary collaboration, and networking, which are particularly attractive and important for young investigators.
Antonio Enriquez, Ph.D., from the Centro Nacional de Investigaciones Cardiovasculares in Madrid, offered a framing of why this meeting stands apart from other conferences in the field:
“The Keystone Symposia meeting explicitly reframes mitochondria from a ‘powerhouse’ housekeeping role into central signaling hubs capable of being tailored for cell type and physiologically changing conditions, shaping cell fate and disease—bringing together basic, translational, and clinical perspectives in one tightly integrated program. In addition to the scientific sessions, the meeting format was designed to maximize cross-career and cross-sector interactions (e.g., poster sessions, a therapy-focused panel, and a dedicated Career Roundtable), making it particularly strong for generating collaborations and for trainees to get targeted career guidance.”
Lena Pernas, PhD, Associate Professor in the Department of Microbiology, Immunology & Molecular Genetics at UCLA and session chair for the Mitochondria Metabolite Signaling session, highlights broad participation:
“The Keystone Mitochondria Signaling in Physiology and Disease showcased talks from researchers who do not traditionally identify as mitochondrial biologists, which brought fresh conceptual approaches to the field. The meeting also highlighted the power of emerging technologies being applied to mitochondrial questions, opening exciting new experimental possibilities. I also very much enjoyed the panel discussions on therapeutic translation, which underscored the impact of mitochondrial research beyond basic biology.”
Mike Murphy, Ph.D., Program Leader at the MRC Mitochondrial Biology Unit and a panelist on the therapy challenges session, appreciates the scientific breadth:
“Some highlights of the meeting were the expansion of metabolic perspectives and regulatory networks on how mitochondria operate in health and disease. Related to this is the development of multiomic approaches and tools, such as that of Dave Pagliarini, that are empowering this next stage in mitochondrial research. The links of these approaches to understanding pathology and potential therapies were also inspiring.”
David J. Pagliarini, Ph.D., HHMI and BJC Investigator, Hugo F. and Ina C. Urbauer Professor, Washington University Medicine, emphasizes the new tools he was exposed to and the value they bring to the field:
“This Keystone meeting featured cutting-edge tool development (e.g., new mitochondrial sensors and screening modalities), new signaling paradigms (via metabolites and PTMs), unexpected mitochondrial interactions with other organelles and external pathogens, and a beautiful summary of where the field stands in our collective quest for new therapeutics.”
Pol Castellano Escuder, Ph.D., a computational biologist and AI researcher currently at the Duke Molecular Physiology Institute (DMPI) and CTO of https://www.heurekalabs.co/, brings a new AI perspective into the mitochondrial research and clinical community.
“Heureka Labs was thrilled to attend the Keystone Symposium on Mitochondria Signaling in Colorado. It was energizing to see the breadth of pathways being explored and the discoveries coming out of this community, and particularly fascinating to watch how so many threads of modern multi-omics research keep converging. As one researcher put it, ‘all roads lead to the mitochondria eventually.’ Between the new tools, methods, and technologies being shared, it’s a genuinely exciting time to study mitochondria and their role in physiology. What the conference also made clear is that data proliferation and the push toward cross-disciplinary integration are outpacing what traditional approaches can handle.
Larissa Govers, a doctoral candidate in the Lab for Retinal Cell Biology at the University of Zurich gave perhaps the most personal account. She presented her work on the metabolic consequences of chronic hypoxia on mitochondrial function in photoreceptor cells:
“What began as a nerve-wracking solo trip across the pond turned into an experience that strengthened my scientific foundation and expanded my network within the field. I left the meeting feeling energized and deeply motivated to continue to grow as a researcher within this collaborative environment. As an early investigator who is relatively new to the field of mitochondrial signaling, attending a conference by yourself specifically focusing on this topic can be an overwhelming experience. There are countless new people to meet and so much to learn from the experts who have shaped the field. Still, deciding to attend this Keystone meeting to deepen my foundation in mitochondrial research was one of the best decisions I could have made.
Beyond the opportunity to expand my knowledge and generate new research ideas, I was blown away by the open culture within this community. I got to meet a lot of new people, and every person I met was inspiring and motivating in their own way. I was particularly grateful for the leaders in the field, who made time to listen to early investigators, gave us direction in our projects, supported us in our career development, and most importantly encouraged us to become the next generation of scientists who will continue advancing mitochondrial research.”
How to Register for the On-Demand Program
The On Demand recordings cover all main-session presentations from the Grays Peak conference room. On Demand Registration here: https://www.keystonesymposia.org/conferences/conference-listing/meeting/pricing/B12026
A multi-institute research group led by Thomas MacVicar at the Cancer Research UK Scotland Institute, Glasgow, found that a specific transporter called SLC25A45 is required for the transport of methylated amino acids across the inner mitochondrial membrane and for carnitine synthesis. This study was published as a recent paper in Molecular Cell 1.
For cellular metabolism to function effectively, metabolites must be exchanged between the mitochondria and the cytosol. Crossing the inner mitochondrial membrane requires the action of transporter proteins. Disruptions to these transporters can lead to disease. The most common transporters are the members of the solute carrier (SLC) 25 family. However, the substrates for some transporters are unknown. Among these “orphan transporters” was solute carrier (SLC) 25A45.
Mitochondria are deeply involved in amino acid metabolism, but the researchers wondered how they deal with methylated amino acids. Disruptions to the systems regulating methylated amino acid homeostasis are associated with heart and kidney diseases, and some are associated with tumors. The team found that a specific transporter, SLC25A45, binds to dimethylarginine and trimethyllysine, but not to the unmethylated version of these amino acids.
Identifying the substrate for orphan transporters is valuable knowledge. SLC25A45 is particularly important for its roles in the transport of methylated amino acids and carnitine biosynthesis. This research also suggests some new possible therapeutic strategies.
A conversation with Dr. MacVicar:
MitoWorld: Can you describe the directions of your research to further the findings of this paper?
MacVicar: Now we know that methylated amino acids enter mitochondria via SLC25A45, we are keen to understand how this pathway impacts cancer progression. The Birsoy and Kajimura labs have shown in mice that mitochondrial uptake of trimethyllysine, and subsequent biosynthesis of carnitine, is important for physiological responses that depend on fatty acid oxidation 2,3. We are employing cancer mouse models to explore how mitochondrial metabolism of trimethyllysine and other methylated amino acids impact tumour growth and survival.
MitoWorld: Do you have any plans to tackle other orphan transporters?
MacVicar: Orphan solute carriers are crucial pieces missing from the mitochondrial metabolism jigsaw. With continued collaborative and creative research, I’m optimistic that each member of the SLC25 family will be deorphanised within 5 years. It will be a challenge though, in part because some orphan transporters appear to have specialised tissue-specific roles. As fun as the SLC25A45 project was, we don’t currently have plans to take on any more orphans ourselves. We have much to learn about the regulation of SLC25 protein biogenesis and activity, and I also think it’s important to study non-SLC25 mitochondrial metabolite transporters. This includes interesting metabolite transport proteins that appear to be dual-localised between mitochondria and other cell membranes. I’m excited to see what comes next from this dynamic field.
MitoWorld: Methylation is a common post-translational modification. Can you speculate on why the mitochondria have become specialized in dealing with some of these?
MacVicar: here may be several advantages of compartmentalising methylated amino acid metabolism. As mentioned, cells can control carnitine biosynthesis by regulating mitochondrial import and hydroxylation of trimethyllysine in the matrix. Whereas mitochondrial sequestration of dimethylarginine perhaps controls nitric oxide synthesis, which is inhibited by cytosolic accumulation of dimethylarginine. By importing methylated amino acids, mitochondria may somehow play a role in sensing the downstream products of methionine metabolism and protein catabolism. Of course, this remains very speculative for now!
MitoWorld: We always wonder how you became interested in mitochondria. Can you expand on that?
MacVicar: I was hooked on mitochondria after some live-cell imaging experiments at the beginning of my PhD. I was surprised and fascinated by the interconnected and dynamic behavior of the mitochondrial network, which was not something I’d gathered from textbooks.
References
- Dias MM, King MS, Shokry E, Lilla S, Paul N, Thomason P, Zanivan S, Sumpton D, Kunji ER, MacVicar T (2025) SLC25A45 is required for mitochondrial uptake of methylated amino acids and de novo carnitine biosynthesis. Molecular Cell 85: 4093–4104.
https://www.cell.com/molecular-cell/pdfExtended/S1097-2765(25)00703-8
- Khan A, Yen FS, Unlu G, DelGaudio NL, Erdal R, Xiao M, Wangdu K, Cho K, Gamazon ER, Patti GJ, Birsoy K (2025) Machine-learning-guided discovery of SLC25A45 as a mediator of mitochondrial methylated amino acid import and carnitine synthesis. Cell Metabolism 37: 2220-32.
https://doi.org:10.1016/j.cmet.2025.09.015
- Auger C, Nishida H, Yuan B, Silva GM, Fujimoto M, Li M, Katoh D, Wang D, Granath-Panelo M, Shin J, Witte R (2026) Mitochondrial control of fuel switching via carnitine biosynthesis. Science 391: eady5532.
The activation of T cells is a critical part of our adaptive immune system. T-cell activation requires massive increases in gene expression and cell proliferation, which is dependent on increased energy production. A research team at the Cancer Research UK Scotland Institute in Glasgow, led by Alison Galloway, Victoria H. Cowling and Tom MacVicar, examined RNA splicing mechanisms involved in T-cell activation. Mitochondria act as a signaling nexus in T cells, and they found that T cells regulate their energetic capacity by alternative splicing of proteins involved in mitochondrial fission and fusion to match the demands of T-cell activation. This study was recently published as a paper in Cell Reports.
More specifically, the team focused on the RNA cap methyltransferase 1 (CMTR1). This enzyme methylates the first nucleotide on mRNAs and U2 small nuclear RNA, part of the spliceosome. Using transcriptomics, they found a splicing module, regulated by CMTR1, that changes the protein isoforms of factors that control mitochondrial fission and fusion. CMTR1 promotes expression of protein isoforms that alter the balance between fusion and fission to produce longer mitochondria in activated T cells. Those longer organelles have greater respiratory capacity.
Thus, the researchers show that increasing CMTR1 levels increases oxidative phosphorylation and supports T-cell activation. This study further shows that mitochondria do more than just produce energy. It also adds to the knowledge of the immune system, the highly complex and crucial mechanisms for our health.
A conversation with Drs. Galloway and Cowling
MitoWorld: Can you give us an idea of the next steps for this research? For example, might you further examine how CMTR1 modulates splicing?
We are interested in how T cells function in tumours. Therapies that improve or support T-cell functions are proving successful in the treatment of many cancers. A limitation of these therapies is that T cells become “exhausted”, exhibiting features associated with loss of mitochondrial quality control, such as depolarized mitochondria and mitochondria with disrupted morphology of the cristae. By targeting CMTR1 and other RNA cap methyltransferases, it is possible that we can support mitochondria function in T cells.
MitoWorld: As you note, mitochondria are involved in many aspects of T-cell biology. Any thoughts on how they might regulate T-cell receptor (TCR) signaling strength, memory formation, or T-cell exhaustion?
Mitochondrial dynamics is a very exciting area in T-cell research. TCR signaling strength is increased by the migration of mitochondria to the immunological synapse—the site at which the TCRs are engaged with antigen/MHC complexes on the antigen-presenting cell. This process is facilitated by mitochondrial fission, which generates smaller, more mobile mitochondria and, thus, is very dependent on mitochondrial fission factors, such as DNM1L/DRP1. On the other hand, memory T cells are metabolically very dependent on oxidative phosphorylation. The longer, more complex mitochondrial networks generated by fusion have greater respiratory capacity, thus the generation and maintenance of memory T cells is very dependent on mitochondrial fusion factors, such as OPA1. Therefore, the proper regulation of T-cell activation, effector function, and memory formation depends on dynamic regulation of mitochondrial morphology, as well as metabolism. In exhausted T cells, we are seeing signs that mitochondrial dynamics have been disrupted, resulting in a buildup of depolarized mitochondria. This is linked to impaired mitophagy, the process by which damaged mitochondria are removed.
MitoWorld: T-cell activation requires careful coordination of gene activation in both the nucleus and mitochondria. Do you have any hypotheses about how this signaling is accomplished?
We think that the RNA cap methyltransferases play important roles in coordinating gene expression and energy production during T-cell activation. After T-cell activation, upregulation of the RNA cap methyltransferase, RNMT, co-ordinates gene expression programmes that results in ribosome production. Ribosomes are the most energy hungry component of the cell; it’s interesting that the genome evolved such that upregulation of another RNA cap methyltransferase—CMTR1—increases respiration during T-cell activation.
MitoWorld: There are hundreds to a few thousand mitochondria in each cell. Do you have any idea about the number or portion of mitochondria must be fused to change the energy production within the cell?
This is a tricky question! In our measurements of mitochondrial length in T cells, we saw a huge range in mitochondrial size with the longest measuring in at nearly 2.5 mm long and the shortest under 0.1 mm. Some of this variation will be due to the orientation of each mitochondrion during the microscopy, but it still indicates that there can be big differences between mitochondria within the same cell. There are still a lot of questions to answer around how the length of the mitochondria influences their metabolic activity.
MitoWorld: T-cell activation is obviously related to infections. Can you envision how your findings might inform therapeutic strategies?
Yes, there are several strategies that may improve or support T cells in tumours, focusing on mitochondria. Mitochondrial functionality could potentially be enhanced by engineering deregulated CMTR1 expression or increasing activating phosphorylation on CMTR1. Alternatively, the splicing modules which control mitochondria function could be more directly controlled in T-cell therapeutics.
MitoWorld: Why did you become interested in mitochondria in the first place? Which came first: mitochondria or the immune system?
VC: My first publication (2002!) was about cytochrome C-triggered caspase cascades. Beyond this, I think there is a fascinating relationship between mitochondria and ribosomes. Gene expression is dependent on energy production by mitochondria supporting energy-hungry ribosomes.
AG: For me, the immune system came first, but the mitochondria are making themselves very hard to ignore since they keep showing themselves to be key mediators of immune cell function!
Reference
Galloway A, Knop K, Gomez-Moreira C, Xavier V, Thomson S, Yoshikawa H, Suska O, Lukoszek R, Kaskar A, Lamond AI, MacVicar T, Cowling VH (2025) CMTR1 directs mitochondrial dynamics during T cell activation through epitranscriptomic regulation of splice isoforms. Cell Reports 44(10): 116412.
The immune system is our first line of defense against cancer. However, tumors have developed mechanisms to evade the immune system and even to invade tumor strongholds, such as lymph nodes. A multi-institute research team led by Azusa Terasaki and Derick Okwan-Duodu explored those mechanisms. They found that tumor cells kidnap mitochondria from immune cells and, in doing so, reduce the effectiveness of those cells. The work was published recently in a paper in Cell Metabolism.
The team was intrigued by the observation that tumor cells often metastasize to the lymph nodes, which are typically well stocked with immune cells. In their study, they first noticed that the immune cells lost mitochondria to the tumor cells.
They next determined what resulted from the loss of mitochondria by the immune cells. In fact, a lot happened, and it was not good for the immune cells. The ability of the immune cells to deal with perceived foreign cells, such as tumor cells, was significantly eroded. Reductions were observed in antigen-presentation, co-stimulatory machinery, and the activation and cytotoxicity of natural killer and CD8 T cells. When the transfer of mitochondria was blocked, the tumor cells could not metastasize to the lymph nodes.
The lymph nodes are common targets of metastases, which might seem counter-intuitive. However, Azusa et al. demonstrate how that happens. The findings of this study have clear clinical implications.
A conversation with Drs. Azusa Terasaki and Derick Okwan-Duodu:
MitoWorld: Can you give us an idea of the research you plan to do to follow up on this study?
We are interested in understanding the fate of the mitochondria once they are acquired by cancer cells. The assumption is that cancer cells will integrate the new biomaterial and use it up. But, can they do something else with it?
MitoWorld: What do you think makes the mitochondria of immune cells vulnerable to kidnapping by the tumor cells in a way that the stromal cells are not?
Answer: We are unsure about this. Please note that many other cell types also transfer mitochondria to cancer. Therefore, the question may not be “why are immune cells vulnerable to mitochondria kidnapping (I love the word choice).” I think it should be, why do cells give mitochondria to cancer anyway? We think cancer, the wound that does not heal, “pretends” to be struggling to elicit mitochondria transfer from other cells as part of normal cooperative biology. Remember, the key theme that is emerging from mitochondria transfer is that is a metabolic rescue program.
MitoWorld: Do you have any thoughts on how the loss of mitochondria impairs the functioning of the immune cells? Is it simply a loss of energy or might it be something else?
Answer: I think it may play a key role. Either the loss of energy, or the disruption from losing mitochondria. Inevitably, the mitochondria has to be disrupted one way or another before they are transferred, and I don’t think immune cells would like that.
MitoWorld: How do the tumor cells attract the immune cell mitochondria, and what mechanism might be used in that transfer?
Answer: No idea. All that is currently known is tunneling nanotubes (predominantly). But it is unclear why cancer cell attracts more mitochondria from cell type A compared to cell type B.
MitoWorld: Other recent papers have described how the transfer of mitochondria to tumor cells fortifies the tumor cells, particularly enhancing their energy levels. You mention several effects on the tumor cells. Can you speculate on how those happen?
Answer: A huge one is indeed metabolic. A highly proliferative cell will use new raw material for whatever their bioenergetic or biosynthetic needs may demand. Nonetheless, mitochondria are also signaling units, and so incoming mitochondria could provide a means of cellular communication beyond metabolism From an espionage perspective, think of a cancer cell now having access to information of the host that is coded in the mitochondria it hijacks. The implications are endless.
MitoWorld: This work would seem to suggest possible clinical applications. Do you have plans to pursue any of them?
Answer: Blocking mitochondria transfer should improve cancer therapies because, at the minimum, you may be shutting off metabolic pipeline to cancer cells while leaving immune cells with a full complement of their metabolic resources, which gives them a better chance to mount effective anti-cancer immunity.
Reference
Terasaki A, Bhatnagar K, Weiner AT, Tan Y, Szeifert V, Huang HL, Wiggers L, Rodrigues V, Rada CC, Shankar V, Saito S, Ankomah PO, Roth T, Chiu B, West R, Li L, Reticker-Flynn N, Axelrod JD, Brestoff JR, Li B, Engleman E, Okwan-Duodu D (2026) Mitochondrial transfer from immune to tumor cells enables lymph node metastasis. Cell Metabolism
https://www.cell.com/cell-metabolism/abstract/S1550-4131(25)00545-5
We welcome Dr. A. Phillip West to the board of directors of the California-based nonprofit National Laboratory for Education Transformation, www.NLET.org. “NLET” is the parent nonprofit of www.MitoWorld.org, our global mitochondrial community web-hub and blog site, and www.mitos.global, our collaborative platform for multi-institution and multi-PI single-subject projects, grants, and funding opportunities.
“We are honored to welcome Phillip to the NLET Board,” said Board Chair David Andrews. “His deep scientific expertise and international research stature will enhance our ability to convene and empower the global mitochondrial research community. Together, we will accelerate discoveries, build collaborative research platforms, and support the translation of mitochondrial science into clinical and societal solutions.”
Dr. West’s leadership, understanding of the growing mitochondrial field, and his scientific credentials will be pivotal in guiding these mitochondrial efforts to benefit the wider mitochondrial research and clinical communities by bringing support, awareness, and new tools to the field.
“I am delighted to join the NLET board at such a pivotal moment for mitochondrial science,” said Dr. West. “We are witnessing a fundamental shift in how mitochondria are understood, not merely as cellular powerhouses, but as central regulators of cellular signaling, immunity, and much more. MitoWorld and MITOS.Global represent exactly the kind of collaborative infrastructure our field needs to increase awareness of mitochondrial biology and translate discoveries into meaningful advances for human health. I look forward to contributing to NLET’s mission of building bridges between researchers, clinicians, and the general public as we work to elevate mitochondrial medicine on the global stage.”
Dr. West is an associate professor and principal investigator at The Jackson Laboratory (JAX) in Bar Harbor, ME. In addition, he serves as a research program co-lead for the NCI-designated JAX Cancer Center, which is focused on understanding the role of aging in cancer development and progression. The West lab explores how mitochondria regulate innate immune and inflammatory responses in health and disease. His team has significantly advanced understanding of mitochondrial DNA (mtDNA) signaling and its influence on disease susceptibility and progression, including inflammatory heart failure, cancer, and rare mitochondrial diseases. He received his PhD in Immunobiology from Yale University and completed postdoctoral training at Yale School of Medicine. Learn more at www.westlaboratory.com. (JAX)
As a member of the NLET board, Dr. West will support strategic efforts to grow NLET’s biomedical informatics and collaboration initiatives. NLET’s MitoWorld™ platform serves as a global web hub connecting researchers, clinicians, and patient advocates to accelerate research and clinical collaboration in mitochondrial medicine. This platform disseminates cutting-edge research, supports patient communities, and fosters interdisciplinary science in mitochondrial health and disease.
Complementing this, NLET will be looking for resources to support frontline research with MITOS.Global as a networked institute devoted to comprehensively understanding mitochondrial biology across health, aging, and disease—integrating basic science with AI-driven informatics and global research collaboration to forge new frontiers in mitochondrial science.
About National Laboratory for Education Transformation
The National Laboratory for Education Transformation (www.NLET.org) is a nonprofit dedicated to innovative research and transformative strategies in education, science, and health. NLET convenes experts and stakeholders across domains to challenge traditional paradigms and advance interdisciplinary research and practice. As part of its mission, NLET fosters initiatives connecting global research communities, with a special focus on emerging scientific priorities, including mitochondrial science and biomedical informatics.
Media Contact:
Gordon Freedman
gordon.freedman@nlet.org
At the Fusion “Mitochondria & Cell Fate Transitions: From Stemness to Senescence” in
St. Julian’s, Malta, May 10–13, the organizers are bringing together are bringing together mitochondrial and STEM cell biologists to better understand cell-fate mechanisms.
The conference organizers, Drs. Mireille Khacho (University of Ottawa), Elisa Motori (University of Cologne), and Maria Eugenia Soriano (University of Padova), will bring together a range of researchers from different disciplines to connect mitochondrial dynamics, metabolism, redox signaling, and organelle communication with cell-fate decisions.
“Lots of exciting mitochondrial research is being done, but it tends to exist in silos,” said Dr. Khacho. “We want to break down those silos to get beyond simple correlations and on to a mechanistic understanding. As the title says, we want to cover mitochondria from stemness to senescence.”
The Conference will bring together leaders across mitochondrial biology, stem cell biology, aging, metabolism, and disease to explore how mitochondrial state actively governs cell fate transitions. Rather than treating mitochondria as passive bioenergetic organelles, the meeting centers on their roles as dynamic regulators of signaling, gene expression, immune crosstalk, and cellular identity across contexts ranging from development and regeneration to degeneration and senescence.
The Conference organizers have multiple goals. They hope to establish new conceptual frameworks for mitochondria-driven cell fate control, enable cross-disciplinary collaborations, and identify new therapeutic possibilities.
Arising frontiers and challenges will be featured. These include understanding the causality between mitochondrial remodeling and fate transitions, how mitochondrial diversity shapes distinct signaling trajectories and functional outcomes, how mitochondrial dynamics connects with transcriptional and epigenetic regulation, how mitochondria-driven senescence programs are distinct from classical damage-induced models, and how single-cell and spatial approaches can be integrated to capture mitochondrial function in vivo.
This meeting is specifically designed for investigators and trainees working in mitochondrial biology and dynamics, stem cell biology and regeneration, aging, senescence, and cell stress responses, cancer cell plasticity and immune–metabolic crosstalk, systems biology, metabolomics, and advanced imaging.
“The conference will be highly interactive plenty of early-career investigators and time for discussion,” said Dr. Khacho. “We hope to see you in Malta.”
For more information and to review the program and confirmed speakers, please visit the Fusion Conference webpage: https://fusion-conferences.com/conference/197.
Questions for the organizers:
MitoWorld: The Conference title (i.e., From Stemness to Senescence) covers a lot of ground. How did you pick the topics and speakers to bring this all together?
Organizers: The title was chosen to reflect both a biological continuum and a physiological trajectory, from normal stemness and regenerative capacity to pathological states, such as dysfunction, degeneration, and senescence. We deliberately selected topics and speakers that sit at key transition points, where cells change identity, competence, or trajectory, because these are moments when mitochondria their roles extending far beyond energy provision to encompass signaling, adaptation, and cell fate determination. Speakers were chosen for both scientific excellence and conceptual complementarity, bringing together perspectives from stem cell biology, aging, cancer, immunity, and neurobiology to create dialogue across traditionally separate fields.
MitoWorld: You have some outstanding goals for the Conference (e.g., “establish new conceptual frameworks for mitochondria-driven cell fate control”). What was the process to arrive at these, and will anyone attempt to synthesize any conclusions from the discussions?
Organizers: The goals emerged from ongoing discussions among the us three co-organizers, where a recurring challenge was the lack of shared frameworks linking mitochondrial changes to cell fate decisions. When FUSION announced the opportunity to propose a new conference topic, it felt like the right moment—a signal, almost—to turn our ongoing informal discussions into a collective effort. Rather than imposing predefined models, we designed the conference to allow concepts to evolve through discussion. We are planning moderated discussion sessions and thematic synthesis moments, and we intend to explore a post-conference summary or perspective to capture key insights, open questions, and future directions.
MitoWorld: Stem cells are a powerful tool, but also a subject in their own right. I understand you have a special connection to STEM cells and mitochondria. How do you hope the conference will be able to differentiate and yet combine these two goals?
Organizers: Stem cells offer a unique lens through which to study plasticity, commitment, and loss of regenerative potential, processes in which mitochondria play an instructive role. The conference does not treat stem cells as a niche topic, nor mitochondria as background machinery. Instead, stem cells are used as a conceptual framework to ask broader questions about how mitochondrial state encodes fate decisions, questions that extend naturally to aging tissues, cancer, and immune cells.
MitoWorld: Mitochondria research has had some controversies, one of which is the split between specific research findings or facts and adding more directly to basic scientific understanding. Do you anticipate that this Conference will provide an opportunity to re-set that balance?
Organizers: Yes. Many translational efforts in mitochondrial biology have been limited by incomplete mechanistic understanding, and we see real value in tightening that connection. This conference emphasizes mechanism-driven biology while remaining grounded in physiological and disease-relevant contexts. By bringing together basic scientists and translational researchers in a highly interactive format, we aim to foster a more integrated approach in which rigorous discovery and meaningful application inform one another.
MitoWorld: What specific provisions have you made to ensure that trainees will have quality time with the more experienced researchers? And in the future is there a way to make these events more accessible and affordable for them?
Organizers: We’ve been fortunate to build on the FUSION format, which inherently supports trainee engagement through its small size, shared meals, and extended discussion periods. This naturally creates space where early career researchers can interact meaningfully with more senior scientists. We further prioritized trainees through short talks selected from abstracts, dedicated poster sessions, “meet the poster presenters” session and informal networking opportunities. We have also worked diligently to secure funds, in the form of travel awards, for trainees and early career researchers.
MitoWorld: This Conference promises to be an outstanding event. What plans do you have to sustain the momentum?
Organizers: We’re pleased that the ambition and enthusiasm we’ve invested in this conference concept are immediately recognizable. We view this conference as the foundation of an ongoing scientific effort rather than a one-time event. Our intention is to establish Mitochondria & Cell Fate Transitions as a recurring meeting held every other year, creating continuity and an evolving forum for the field. Between meetings, we aim to sustain momentum through continued engagement via platforms such as MitoWorld. This structure allows ideas, debates, and emerging frameworks to mature over time while keeping the community connected and forward-looking.
Conference Organizers:
Mireille Khacho (University of Ottawa) investigates how physiological changes in mitochondrial dynamics and metabolism regulate stem cell fate, function, and regeneration. Her work focuses on mitochondrial-dependent metabolite and redox signaling in physiological contexts, and how disruption of these pathways drives neuromuscular diseases, aging and mitochondria-driven senescence.
Elisa Motori (University of Cologne) investigates how cell type–specific mitochondrial and metabolic programs shape brain health and disease vulnerability, revealing energy-driven mechanisms that govern development, resilience, and neurodegeneration.
Maria Eugenia Soriano (University of Padova) investigates how mitochondrial structure and dynamics are transcriptionally regulated to shape cellular metabolism. Using physiological and disease-relevant models, her work integrates mitochondrial biology, metabolic regulation, and gene expression to uncover how alterations in mitochondrial organization drive metabolic rewiring in cancer and other pathologies.
MitoWorld.org and MITOS Global have announced a new partnership with Heureka Labs, an AI-driven discovery platform with roots at Duke University, aimed at fundamentally expanding the analytical and discovery capacity of the global mitochondrial research community.
The collaboration brings together MitoWorld’s role as an organizing and convening force in mitochondrial science with Heureka’s advanced agentic research infrastructure, designed to support hypothesis generation, multi-omic analysis, and translational insight at scale.
“The mitochondrial research community has extraordinary biological insight, but it has largely lacked access to modern, integrated computational discovery systems,” said Gordon Freedman, Founder and President of the National Laboratory for Education Transformation (NLET), the nonprofit organization that operates MitoWorld and MITOS Global. “This partnership gives mitochondrial researchers discovery, analysis, and hypothesis-generation capabilities that have not previously existed in this field.”
Addressing Fragmentation in Mitochondrial Science
Mitochondria sit at the center of energy production, cellular signaling, metabolism, immunity, aging, and disease. Yet mitochondrial research remains highly fragmented across institutions, disease areas, and data silos. MitoWorld and MITOS Global were created specifically to address this fragmentation, building shared infrastructure for collaboration, translation, and synthesis across the field.
The addition of Heureka Labs introduces a powerful computational layer to that mission.
“This partnership represents exactly the kind of transformative collaboration we envisioned when building the Heureka platform,” said Dr. Matthew Hirschey, Professor at Duke University, Director of the Duke Center for Computational Thinking, and co-founder of Heureka Labs. “By combining MitoWorld’s deep domain expertise in mitochondrial research with our advanced computational capabilities, we’re not just organizing existing knowledge. We’re creating a powerful engine for scientific discovery that can accelerate breakthrough research in this emerging field.”
Augmenting, Not Replacing, Experimental Science
Through the partnership, MITOS Global researchers will gain access to Heureka’s agent-based research environment, which integrates scientific literature, biological databases, and computational analysis into a unified workflow. The platform is designed to augment and catalyze existing scientific processes—allowing researchers to explore complex hypothesis spaces, test data-driven connections, and identify promising directions before committing time and resources in the laboratory.
The partners emphasize that experimental science remains central to discovery. Computational exploration is used to guide, refine, and strengthen laboratory investigation and not substitute for it.
Heureka Labs has already been adopted by biotechnology companies, universities, and research institutes across the United States, Europe, and Asia. The MITOS Global partnership represents a focused application of this platform to one of the most biologically and clinically significant domains in modern science.
This builds on parallel efforts that leveraged Heureka’s data models to successfully uncover unexpected interactions across genes and pathways, leading to recently published discoveries relating to cancer research.
What This Means for Researchers
For mitochondrial researchers, the partnership provides access to consolidated multi-omic datasets, automated and reproducible bioinformatics workflows, and same-day analytical capabilities that previously required weeks or months of effort. The platform supports tasks ranging from transcriptomic and metabolomic analysis to pathway mapping, target prioritization, and biological interpretation, all within a unified research environment.
Importantly, the system is designed to serve laboratories with varying levels of computational expertise. Advanced users can directly engage with analytical pipelines and annotated code, and labs with limited bioinformatics capacity can interact through guided workflows and plain-language prompts. This flexibility reduces dependence on external contract research organizations and overburdened core facilities, lowering costs while expanding access to high-quality computational analysis.
Beyond efficiency gains, the partnership enables a qualitative shift in how mitochondrial research is conducted. By centralizing data in the MITOS environment and enabling real-time insight sharing across institutions, the platform supports collective learning rather than isolated discovery. As new findings are generated within MITOS Global projects, they enrich a growing knowledge base that strengthens future analyses and uncovers previously hidden biological relationships.
Heureka’s platform also supports downstream translational activities, including grant development, manuscript drafting, and review preparation, ensuring that insights generated through computational exploration can be efficiently communicated and validated. This integrated approach improves research quality while reducing administrative and analytical bottlenecks.
Initial Joint Project: A Mitochondria-Cancer Atlas
As part of the partnership, MitoWorld.org and Heureka Labs also announced an initial early-stage project to develop a Mitochondria-Cancer Atlas. This effort is designed to catalog the diverse ways cancers adapt, reprogram, and exchange mitochondria to support tumor growth, survival, and therapeutic resistance. The project will apply advanced computational analysis to one of cancer biology’s most complex and rapidly expanding frontiers: mitochondrial plasticity in cancer, with the goal of sharing insights across the broader mitochondrial and medical communities.
“Cancer provides the best living laboratory for the range of behaviors and manipulations that can happen to mitochondria in a living context,” said Alexander Sercel, PhD, MitoWorld’s Director of Scientific Affairs. “Cataloging these in a comprehensive way should lead to deeper levels of understanding of the basic science of mitochondria.”
Partnership Structure
The primary agreement for this partnership is between Heureka Labs and the National Laboratory for Education Transformation (NLET), the parent nonprofit organization that operates both MitoWorld and MITOS Global.
Information: Heureka Labs
In a recent paper in Nature Metabolism, an international research group, used a new multi-gene approach to pathway mapping to identify complex II as a central regulator of de novo purine biosynthesis and a promising therapeutic target for acute myeloid leukemia.
Understanding genetic pathways is important in biology and medicine. However, complex diseases, such as cancer, might involve interactions between different pathways that are not immediately obvious. While much work has been done in understanding how individual genes interact, less is known about how multi-gene pathways interact.
Now a team, led by Matthew Hirschey and Kris Wood of Duke University and Alexandre Puissant of the Saint-Louis Research Institute/Hospital, INSERM in Paris, have developed a tool that can look for interactions between pathways. Specifically, they developed novel computational methods to examine genetic pathways involved in acute myeloid leukemia.
Interestingly, they discovered an unexpected link between complex II and purine metabolism with glutamate as a key intermediate. This observation implicates complex II as a potential therapeutic target. AML patients with higher complex II expression have worse survival rates.
These findings clearly demonstrate the power of data-driven tools for identifying critical interactions between genetic pathways. They also show the value this approach for finding possible new therapeutic strategies.
A conversation with Dr. Hirschey
MitoWorld: Congratulations on taking this next step in systems biology. Have you received any feedback from others in the field about it?
Hirschey: Thank you. The response has been very positive, particularly from colleagues working on cancer metabolism. Many have noted that our pathway-level approach fills a gap; while gene-gene coessentiality has been powerful, the emergent properties of pathways working together were being missed. Several groups have already started using our web tool at datadrivenhypothesis.org to explore their own systems of interest.
MitoWorld: Your work yielded surprising connections for glutamate and complex II. Do you have any other systems in mind to look at with this new tool?
Hirschey: Absolutely. Our analysis revealed Complex II has additional unique pathway connections that other ETC complexes don’t share. Beyond nucleotide metabolism, we saw strong links to amino acid pathways, particularly aspartate and glutamine metabolism. We’re interested in exploring how other TCA cycle enzymes might have similar “moonlighting” functions. Recent work from other groups on OGDH and fumarate hydratase suggests this is a rich area.
MitoWorld: You note several reasons that complex II is a possible therapeutic target in AML. Do you have any plans to follow up this line of research?
Hirschey: Yes, we’re actively pursuing this. Our data showing that Complex II inhibition sensitizes AML cells to venetoclax are particularly exciting given venetoclax resistance is a major clinical problem. We’re working on in vivo pharmacological studies and exploring synergistic strategies.
MitoWorld: Complex II may indeed be a target for AML and some other cancer. Can you speculate on whether it might be for a broader range of cancers?
Hirschey: Our pan-cancer analysis suggests caution here. High SDHB expression significantly increases mortality risk in only two cancer types, with AML being one. This contrasts sharply with pheochromocytoma and renal cancers, where Complex II acts as a tumor suppressor. So this isn’t a “one-size-fits-all” target. That said, our data point to broader vulnerability in hematolymphoid malignancies, where B-ALL, DLBCL, and anaplastic large cell lymphoma all showed Complex II dependency.
MitoWorld: In your discussion, you mention the increasing number of non-canonical functions of the mitochondria that have been found in recent years. Can you speculate on others that might be awaiting discovery?
Hirschey: I think we’re just scratching the surface. The TCA cycle has traditionally been viewed as an energy-producing pathway, but it’s clearly a biosynthetic hub with sensing functions. The finding that both FH deficiency and SDH inhibition suppress purine synthesis through metabolite accumulation suggests mitochondria may act as metabolic sensors, detecting imbalances through substrate buildup. I suspect we’ll find more examples where TCA intermediates serve as signaling molecules regulating distant pathways.
MitoWorld: We are obviously interested in mitochondria, but do you have any plans to examine pathways not involved with mitochondria?
Hirschey: Our pathway coessentiality tool is agnostic and can examine any gene set provided. We’ve already looked at transcription factor targets and cell-type signatures beyond metabolism. I’m particularly interested in how metabolic pathways connect to epigenetic regulation, given the known links between TCA metabolites, such as succinate and α-ketoglutarate to chromatin-modifying enzymes. The tool is publicly available, so we hope others will explore non-mitochondrial systems as well.
Reference
Stewart AE, Zachman DK, Castellano-Escuder P, Kelly LM, Zolyomi B, Aiduk MDI, Delaney CD, Lock IC, Bosc C, Bradley J, Killarney ST, Stuart JD, Grimsrud PA, Ilkayeva OR, Newgard CB, Chandel NS, Puissant A, Wood KC, Hirschey MD (2025) Pathway coessentiality mapping reveals complex II is required for de novo purine biosynthesis in acute myeloid leukaemia. Nat Metab 7: 2474–2488 (2025). https://doi.org/10.1038/s42255-025-01410-x.
Get ready for the Cell, Multifaceted Mitochondria Symposium, this year in Glasgow, Scottland, June 21–23.
Like its five biennial predecessors, the Glasgow gathering features the hallmark of the Multifaceted Mitochondria Symposia—a broad and deep array of mitochondrial topics and talks, covering a number of areas of inquiring, including mitochondrial biochemistry and bioenergetics, mitochondria homeostasis and stress response, mitochondrial dynamics and transfer, mitochondrial communication, mitochondria in metabolism, and mitochondria in inflammation and disease. The 2026 event is organized by Isha Jain, Arc Institute and Gladstone/UCF and Thomas Langer, Max Planck Institute for the Biology of Ageing.
Keynotes
Keynote include Judy Hirst, University of Cambridge, and Jared Rutter, University of Utah.
Hirst is a British chemist and mitochondrial biologist at the University of Cambridge, where she is Director of the MRC Mitochondrial Biology Unit and Professor of Biological Chemistry. She leads research into the structure and mechanisms of mitochondrial respiratory enzymes, particularly respiratory complex I, using biochemical and structural methods to understand energy conversion. Hirst is a Fellow of the Royal Society and Fellow of the Academy of Medical Sciences, recognized for her contributions to mitochondrial biology.
Rutter is Distinguished Professor of Biochemistry and holds the Dee Glen and Ida Smith Endowed Chair for Cancer Research at the University of Utah where he has been on the faculty in the Department of Biochemistry since 2003. In 2015, Dr. Rutter was appointed as an Investigator of the Howard Hughes Medical Institute. The Rutter laboratory has identified the functions of several previously uncharacterized mitochondrial proteins, including the discovery of the long-sought mitochondrial pyruvate carrier.
History
The Cell Symposia series on Multifaceted Mitochondria, inaugurated in 2015 in Chicago, has charted the dynamic evolution of mitochondrial research over the past decade. The inaugural meeting focused on foundational themes, such as mitochondrial metabolism and bioenergetics, signaling pathways, mitochondrial dynamics, mitophagy, and quality control. The meeting brought together leaders exploring both basic mitochondrial functions and their intersections with disease, setting a strong mechanistic foundation for the field.
Since then, the symposium has progressively broadened its scope to capture the expanding complexity of mitochondrial biology. By 2022, Jodi Nunnari was the keynote, and the program integrated emerging topics, including mitochondrial communication with other organelles and immune signaling, mitochondrial proteostasis, and the role of mitochondria in inflammation and cancer metabolism. In 2024, several of the www.MitoWorld.org Scientific Advisory Board featured a MitoWorld Initiative. The latest 2026 program anticipates an even wider lens, framing mitochondria as central metabolic and signaling hubs influencing organismal homeostasis, aging, and multi-system diseases. This evolution reflects not only scientific advances but also a growing recognition of mitochondria as versatile regulators and therapeutic targets, a narrative underscored by recurring contributions from influential researchers.
Symposium organizers
Salvatore Fabbiano, Editor-in-Chief, Cell Metabolism, received his PhD in Physiology at the University of Salamanca, where he studied signaling pathways involved in cardiometabolic diseases. He then moved to the University of Geneva to work on host-microbiota homeostasis. He joined Cell Press in 2018.
Shawnna Buttery, Editor-in-Chief, Cell Reports, whose training in the laboratory was in cell biology, studying the cytoskeleton in nematodes as a graduate student at Florida State University and as a postdoc at Dana-Faber Cancer Institute. She has been with Elsevier/Cell Press since 2012.
Thomas Langer, academic co-organizer, who since 2018, has been Director at the Max Planck Institute for the Biology of Ageing in Cologne, focusing on the analysis of mitochondrial proteostasis and its regulation in ageing and age-associated diseases. Langer earned his PhD from the LMU Munich working on chaperone-mediated protein folding and was a researcher at the Memorial Sloan Kettering Cancer Center in New York and professor at the University of Cologne, where he studied the role of mitochondrial protein quality control in neurodegeneration.
Isha Jain, academic co-organizer, associate investigator at the Gladstone Institutes, as well as an assistant professor at UC San Francisco. Jain received her undergraduate degree in chemical and physical biology from Harvard University. There, she worked in the lab of Erin O’Shea on bacterial chromosome segregation. Subsequently, she joined the Harvard-MIT Program in health sciences and technology. She earned a PhD in computer science and systems biology and worked in the labs of Vamsi Mootha and Warren Zapol, where she made the discovery that hypoxia could serve as a therapy for mitochondrial disorders.
MitoWorld Interview
MitoWorld: What makes our Multifaceted Mitochondria meeting unique?
Fabbiano: The mitochondria field is extremely diverse, with researchers working on this organelle from signaling, structural, and bioenergetic perspectives and investigating how they affect cellular, tissue and whole-body homeostasis. This variety of angles is then put in the context of communicable and non-communicable diseases, spanning from the response to infections to metabolic and autoimmune disorders, cancer and aging.
Buttery: Multifaceted Mitochondria stands out because it embraces the full diversity of mitochondrial biology. It offers a comprehensive, top-to-bottom perspective on mitochondria, while bringing together a diverse group of scientists from across the field. This conference strikes a great balance of fresh perspectives and established expertise.
Jain: Because the symposium is intentionally small and highly interactive, you don’t just hear about exciting science; you immediately start brainstorming with the people behind it. That intimacy accelerates collaborations and often launches entirely new directions.
MitoWorld: Is there a risk of being too inclusive, with too many subjects? On the other hand, the field is still emerging. How do you strike a balance?
Fabbiano: The natural risk of such a broad field is thus the breaking down into silos and overspecialization, with each subfield narrowing down their perspective on the individual questions they are answering. Our vision and mission with this meeting are instead to go in the opposite direction, and we make it clear starting from the title: mitochondrial research is multifaceted, and should be appreciated as such to truly push the field forward. What makes us unique is our ongoing mission of strengthening the ties of a diverse community to create new channels of communication, new forms of collaboration, and develop ideas throughout a conference that welcomes both established leaders and emerging voices in the field.
Jain: Multifaceted Mitochondria is the rare meeting where every dimension of mitochondrial biology comes together—from metabolism and genetics to disease and therapy. It’s a unique opportunity to see the whole field at once and spark ideas that wouldn’t emerge in siloed settings.
MitoWorld: For the Glasgow symposium, what did you concentrate on. How did you determine the strands and the array of speakers? What do you hope people come away with?
Langer: It was of utmost importance to us to develop a program that only allows leading experts to discuss their most recent discoveries but also offers plenty of opportunities for young scientists to present their work and interact with other scientists in the field. We hope that the attendees will experience a vibrant and interactive scientific community and will leave with new tools, ideas and collaborators to further push forward the mitochondrial field.
Jain: Mitochondrial biology is advancing at an incredible pace, and this meeting is built to capture that momentum. We want participants to leave with new tools, new collaborators, and a clear sense of the frontier we’re all pushing toward.MitoWorld: What do you find exciting and challenging about organizing a Multifaceted Mitochondria Symposium, given the complexity of the fast-growing field and its many facets?
Langer: It is an exciting possibility and fun to bring together scientists working on different aspects of mitochondrial biology in a small and interactive setting to exchange their discoveries and ideas for new research directions. If I must mention something challenging, then that it is to select speakers among the many excellent scientists to build a program that covers the many aspects of mitochondrial biology and that allows us to identify synergies as a basis for future collaborations.
MitoWorld: It is refreshing to have a leading journal, in this case Cell Metabolism, take on a whole field-in-the making. It sounds like the journal has a hands-on approach with its communities.
Fabbiano: One point that makes us unique is the editorial involvement at these conferences, not only in the organization but in our very presence and engagement with the community. We appreciate that publishing can be a complex experience, and part of our mission with these conferences is also the direct contact with the community to address misconceptions and pain points around peer review and scientific publishing
MitoWorld: Given that approach, how do you interact with the research community in the journal and for a symposia, such as the Multifaceted Symposium?
Buttery: Our meetings are organized by and for the readers, authors, and reviewers that make our journals possible. They reflect the latest directions of the field, address controversies, and are curated in content and size to ensure that everyone from a young graduate student to a tenured professor learn something new and go back to their project with renewed enthusiasm and passion. That is definitely the case for us editors, too.
Important Deadlines:
Abstract submission deadline: February 13, 2026
Early registration deadline: April 10, 2026