Could fixing mitochondria restore insulin-producing cells?
Mitochondria - the tiny power plants inside our cells may be a master switch in diabetes, controlling not just energy production but the very identity of key metabolic cells.
Core finding:
University of Michigan researchers lead by EMILY M. WALKER and team show that when mitochondria are damaged in insulin-producing pancreatic β-cells, a specific cellular stress response switches on, causing these cells to become “immature,” produce too little insulin, and essentially stop functioning as true β-cells. Crucially, the team finds that this same mitochondrial stress program can also be triggered in liver and fat cells, hinting at a unifying mechanism behind the multi-organ breakdown seen in diabetes.
How they tested it::
Using mice, the scientists disrupted three separate pillars of mitochondrial health: mitochondrial DNA, the pathway that clears damaged mitochondria, and the system that keeps a healthy pool of mitochondria in the cell. Despite these different hits, each manipulation triggered the exact same stress response and led β-cells to lose maturity and insulin output, revealing a common “danger signal” from mitochondria to the cell nucleus.
Beyond the pancreas:
Because diabetes affects far more than the pancreas, the team repeated the experiments in liver cells and fat-storing cells, again seeing the same stress response and impaired cell maturation and function. Senior author Scott Soleimanpour notes that losing β-cells is the most direct route to type 2 diabetes, but these results suggest a shared mitochondrial glitch across tissues could be the deeper root cause.
A possible way to reverse it:
In a hopeful twist, mitochondrial damage did not kill the cells, raising the possibility that their function could be restored. When the researchers treated mice with ISRIB, a drug that blocks the stress response pathway, β-cells regained their ability to control blood sugar within four weeks, effectively reversing the mitochondrial-driven dysfunction in this model.
What’s next:
The team confirmed key findings in human pancreatic islet cells and is now dissecting the disrupted pathways in more detail, aiming to repeat the rescue in cells from people with diabetes. If successful, targeting this mitochondrial stress signaling could shift diabetes treatment from managing blood sugar to correcting a fundamental cellular error – turning the cell’s “powerhouse” into a therapeutic entry point.
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About Image
A retrograde mitochondrial signaling cascade induces the loss of identity and maturity in metabolic tissues.
Numerous defects in the mitochondrial quality control machinery are capable of eliciting defects in the ETC-OXPHOS system, which acts as a retrograde signal to trigger the mtISR. Engagement of the mtISR induces chromatin remodeling and transcriptional and functional immaturity in metabolic tissues. TCA, tricarboxylic acid; ADP, adenosine 5′-diphosphate; ATP, adenosine 5′-triphosphate; BAT, brown adipose tissue. [Figure created with BioRender.com]
Referance
DOI: 10.1126/science.adf203
We are pleased to announce that the 17th Conference Targeting Mitochondria 2026 will be held in Berlin, Germany, from October 21-23. We look forward to welcoming you.
Nanoflowers help cells share mitochondria and restore energy
Scientists at Texas A&M University have developed an unusual tool to help damaged and aging cells recover their energy: microscopic particles called “nanoflowers.” These tiny structures can stimulate stem cells to produce and share mitochondria with neighboring cells, restoring cellular energy production.
Mitochondrial decline is a central feature of aging, neurodegeneration, and cardiovascular disease. When cells lose mitochondria, their ability to produce energy drops, leading to reduced function and increased vulnerability to stress.
In this new study, researchers combined stem cells with flower-shaped nanoparticles made of molybdenum disulfide. The particles stimulated stem cells to produce about twice as many mitochondria as normal. These “mitochondrial bio-factory” cells then transferred the extra mitochondria to nearby damaged or aging cells.
The results were striking: recipient cells recovered energy production, improved survival, and resisted stress-induced cell death, including damage from chemotherapy like conditions.
While cells naturally exchange mitochondria at low levels, the nanoflower approach increased mitochondrial transfer by two- to four-fold, suggesting a way to amplify a natural repair mechanism rather than replace it.
Because the nanoparticles remain inside cells longer than conventional small molecule treatments, the approach could potentially enable long-lasting mitochondrial support therapies with less frequent dosing.
Although still at an early stage, the technology points toward a new regenerative strategy: boosting mitochondrial sharing between cells to restore tissue energy and resilience. Researchers suggest this approach could eventually be explored for conditions ranging from cardiomyopathy to neurodegenerative disease and muscle degeneration.
For the mitochondrial field, the study reinforces a growing idea: mitochondria are not only intracellular powerhouses, they are also transferable biological resources that can support tissue repair and cellular recovery.
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About Image
Microscopic image showing how nanoflowers (white) help healthy cells (yellow) deliver energy-producing mitochondria (red) to neighboring cells. Nuclei are stained blue.
Courtesy Dr. Akhilesh K. Gaharwar.
Referance
Texas A&M University (2025). Texas A&M scientists use "nanoflowers" to recharge aging and damaged cells.
We are pleased to announce that the 17th Conference Targeting Mitochondria 2026 will be held in Berlin, Germany, from October 21-23. We look forward to welcoming you.
Cells share mitochondria to protect nerves from pain When cells share mitochondria, nerve pain can be reduced
A new study supported by the National Institutes of Health (NIH) shows that mitochondrial transfer between cells can protect nerves from pain-causing damage, revealing a promising therapeutic strategy for peripheral neuropathy.
Peripheral neuropathy often caused by chemotherapy or diabetes occurs when sensory neurons lose healthy mitochondria and can no longer produce enough energy to function properly. This leads to pain, weakness, and nerve dysfunction.
Researchers discovered that satellite glial cells, which surround sensory neurons in structures called dorsal root ganglia, can transfer mitochondria directly to neurons through tiny cellular bridges known as tunnelling nanotubes.
This mitochondrial transfer proved essential for nerve health. When scientists disrupted the formation of nanotubes or reduced levels of the motor protein MYO10, mitochondrial transfer declined and pain sensitivity increased in mice.
Encouragingly, restoring mitochondrial transfer reversed these effects. Injecting healthy satellite glial cells or even isolated mitochondria into affected nerve regions reduced pain sensitivity in mouse models of diabetic neuropathy and chemotherapy-induced nerve damage.
Human tissue samples showed similar biology: supporting cells from healthy donors displayed stronger mitochondrial-transfer capacity than those from people with diabetes.
Together, the findings highlight a growing concept in mitochondrial medicine: mitochondria can act as transferable therapeutic units, capable of restoring cellular energy and function in damaged tissues.
If translated clinically, strategies that enhance mitochondrial transfer or deliver healthy mitochondria could open a new path for treating chronic nerve pain and neurodegenerative conditions.
One of the hit topic of Targeting Mitochondria 2026 is Mitochondria Transfer and clinical impacts.
Click here for more information.
Image Credit
Scientists found that specialized cells, called satellite glial cells, can transfer mitochondria (red) to neurons through thin nanotubes that connect the two cells.
Ru-Rong Ji lab, Duke University School of Medicine
Referance
Mitochondrial transfer from glia to neurons protects against peripheral neuropathy. Xu J, Li Y, Novak C, Lee M, Yan Z, Bang S, McGinnis A, Chandra S, Zhang V, He W, Lechler T, Rodriguez Salazar MP, Eroglu C, Becker ML, Velmeshev D, Cheney RE, Ji RR. Nature. 2026 Jan 7. doi: 10.1038/s41586-025-09896-x. Epub ahead of print. PMID: 41501451.
We are pleased to announce that the 17th Conference Targeting Mitochondria 2026 will be held in Berlin, Germany, from October 21-23. We look forward to welcoming you.
A Mitochondrial Protein May Hold the Secret to Longevity
Researchers from the Tokyo Metropolitan Institute for Geriatrics and Gerontology have identified a mitochondrial protein that may play an important role in healthy aging. The study focuses on COX7RP, a protein involved in organizing mitochondrial respiratory supercomplexes, structures that improve cellular energy production efficiency.
Mitochondria are central to aging biology because they produce ATP, the energy required for cellular function. Declining mitochondrial performance is strongly associated with aging and age-related diseases. By increasing COX7RP levels in experimental models, researchers were able to improve mitochondrial efficiency, enhance metabolic health, and extend lifespan in mice.
The findings suggest that longevity may depend not only on metabolic activity itself, but on how efficiently mitochondrial systems are organized and coordinated. Respiratory supercomplexes appear to optimize electron transfer and reduce oxidative stress, helping cells maintain energy balance over time.
This work reinforces a growing idea in longevity science: aging is closely linked to the progressive decline of mitochondrial function and biological coordination. Improving mitochondrial organization and efficiency may therefore represent a promising strategy for extending healthspan.
The study also highlights how mitochondrial architecture, metabolism, and redox balance interact to influence aging trajectories, themes that resonate strongly with the systems-biology perspective explored at Targeting Longevity.
The World Mitochondria Society will organize 2 meetings dedicated to mitochondria dynamics next April & October.
Click here for more information.
Image Credit
Title: Exploring the link between COX7RP, a mitochondrial protein, and longevity
Caption: In a new study, researchers from Japan demonstrate that COX7RP, a mitochondrial protein, may play a key role in enhancing mitochondrial energy efficiency, leading not only to longer lifespans but also an extended "healthspan" via numerous health benefits.
Credit: Dr. Satoshi Inoue from Tokyo Metropolitan Institute for Geriatrics and Gerontology, Japan
Referance
Title of original paper: Mitochondrial Respiratory Supercomplex Assembly Factor COX7RP Contributes to Lifespan Extension in Mice
Journal: Aging Cell
DOI: 10.1111/acel.70294
We are pleased to announce that the 17th Conference Targeting Mitochondria 2026 will be held in Berlin, Germany, from October 21-23. We look forward to welcoming you.
Sugar first, mitochondria later: how brain immune cells respond to injury
When the brain is injured, its immune cells don’t wait around. New research reveals that microglia, the brain’s resident immune cells, launch their first response using sugar-based energy, long before mitochondria enter the scene.
Using advanced live imaging, scientists observed that microglia rush toward damage and begin their work almost immediately even though their long cellular extensions contain few or no mitochondria at this early stage. Instead, these cells rely on glycolysis, a fast way to generate energy from sugar, allowing them to move quickly and react within minutes.
Only later do mitochondria arrive. Hours after the initial response, microglia reorganize their internal architecture, building microscopic transport routes that allow mitochondria to travel to the most active zones. Once there, mitochondria support sustained functions such as debris clearance and longer-term immune activity.
This two-step strategy challenges the traditional view of mitochondria as constant power suppliers. Instead, it shows that brain immune cells are metabolically flexible, choosing speed first and endurance second.
Why this matters: microglia play a central role in aging, neuroinflammation, and neurodegenerative diseases. Understanding how healthy microglia manage energy over time helps researchers identify what may go wrong in chronic brain disorders and how mitochondrial function might be restored or optimized.
In short, the brain’s immune response is not only fast it is smart, adaptive, and precisely timed.
The World Mitochondria Society will organize 2 meetings dedicated to mitochondria dynamics next April & October.
Sources & More Information
-
Pietramale AN et al.
Mitochondria are absent from microglial processes performing surveillance, chemotaxis, and phagocytic engulfment.
Nature Communications, 2025.
DOI: 10.1038/s41467-025-66708-6 -
Espinoza K et al.
Dynamic changes in mitochondria support phenotypic flexibility of microglia.
Nature Communications, 2025.
DOI: 10.1038/s41467-025-66709-5 -
MedicalXpress / Dartmouth College (Video and more information)
Brain immune cells arrive powered by sugar, then build roads to recruit reinforcements.
January 26, 2026.
https://medicalxpress.com/news/2026-01-brain-immune-cells-powered-sugar.html
Exercise May Help the Brain Heal After Stroke
New research shows movement can send energy to damaged brain cells, opening new doors for therapy
Exercise has long been known to help people recover after stroke. Now scientists have found a possible reason why. A new study shows that physical activity may help the body deliver energy directly to injured parts of the brain, supporting repair and recovery.
The research suggests exercise is not only training muscles or improving balance. It may activate a natural healing process inside the body that helps brain cells survive and function after injury.
What they did
Researchers studied stroke in mice to closely observe what happens inside the body during recovery. They divided the animals into two groups. One group exercised regularly. The other group did not.
The scientists focused on mitochondria, the parts of cells that produce energy. They measured mitochondria in muscles, blood, and brain tissue.
They found that exercise increased the number of mitochondria in the blood. Platelets then carried these mitochondria through the bloodstream. After stroke, the mitochondria traveled into damaged areas of the brain and entered brain cells.
The researchers also tested movement, memory, and brain structure. Mice that exercised had less damage to brain tissue and performed better on recovery tests.
Why it matters
Stroke treatment options are limited. Emergency care can restore blood flow, but long term brain repair remains difficult. Rehabilitation depends largely on repeated physical practice.
This study adds a new layer of hope. It suggests exercise may work as a biological therapy, helping the brain at a cellular level, not only through practice and training.
Impact
The findings point to a new way of thinking about recovery. Exercise may act as a delivery system, sending energy from the body to the injured brain. This could help explain why movement improves outcomes even weeks or months after stroke.
The research also raises important questions. Could future therapies copy the benefits of exercise for patients who cannot move easily? Could similar approaches help people with dementia or other brain conditions?
Perspective
The study was done in animals, not humans, and more research is needed before clinical use. But the message is optimistic and grounded in biology.
The body is not passive after injury. With movement, it may activate its own repair tools.
Exercise may be more than rehabilitation. It may be part of the medicine itself.
These findings resonate strongly with the spirit of Targeting Mitochondria 2026, where dynamism is the central concept.
They remind us that health and recovery are not static processes, but living, energy-driven dialogues between organs, cells, and systems.
At TM2026, scientists, clinicians, and innovators will explore how movement, energy transfer, and mitochondrial intelligence can reshape our understanding of therapy from stroke recovery to neurodegeneration, aging, and resilience.
This study reinforces a simple but powerful idea: when biology moves, healing follows.
And sometimes, the most effective therapies begin not with drugs, but with restoring the natural dynamics of life itself.
Click here to read more
References & Image Credits:
Inaba T. et al. (2026). Mitochondrial intercellular transfer via platelets after physical training exerts neuro-glial protection against cerebral ischemia. MedComm.
DOI: 10.1002/mco2.70590
Image title: Exercise-induced mitochondria aid recovery from cerebral ischemia
Image caption: Researchers have demonstrated how mitochondria, which are abundant in muscle, could aid in stroke recovery through exercise-induced migration.
Image credit: Dr. Toshiki Inaba, Juntendo University School of Medicine, Japan
We are pleased to announce that the 17th Conference Targeting Mitochondria 2026 will be held in Berlin, Germany, from October 21-23. We look forward to welcoming you.
Concluding Remarks of WMS 2025
The 16th World Congress on Targeting Mitochondria marked a defining moment for the mitochondrial community. Over three days in Berlin, the discussions made one thing clear: mitochondria are no longer a niche topic of cell biology, they have become a central pillar of modern medicine. In his concluding remarks, Marvin Edeas, Founder and Chairman of the World Mitochondria Society, emphasized that mitochondrial research has entered a new phase.
WMS 2025 Awards – Celebrating Scientific Excellence in Mitochondrial Medicine
At Targeting Mitochondria 2025, the World Mitochondria Society honored three outstanding scientific contributions that perfectly reflect the spirit of WMS: bold ideas, rigorous science, and a dynamic vision of mitochondria. These awards celebrate discoveries that connect energy, communication, metabolism, and resilience, reminding us that mitochondria are not static structures, but active players shaping health, disease, and longevity.
Targeting Mitochondria 2025, A Record-Breaking Edition Defining the Next Frontier of Medicine
The World Mitochondria Society (WMS) proudly announces an unprecedented level of participation at the 17th World Congress on Targeting Mitochondria, uniting more than 237 academic and institutional partners and over 31 industrial and investment organizations.
This year’s edition represents a turning point in mitochondrial science, where fundamental biology meets translational medicine, biotechnology, and AI-driven innovation. From energy metabolism to organelle communication, mitochondria are emerging as strategic integrators of cellular function, systemic health, and longevity.
“Mitochondria are no longer seen only as the cell’s powerhouse,” said Volkmar Weissig and Marvin Edeas, President and Founder of the WMS.
“We are now decoding their language, how they communicate, adapt, and influence other organelles. This knowledge is redefining how we approach diagnostics, therapeutics, and prevention.”
With record-breaking attendance and scientific diversity, Targeting Mitochondria 2025 will feature:
Australia:
· Deakin University
Belgium:
· ORBI team, URBC, University of Namur
Brazil:
· University of Campinas (UNICAMP)
Bulgaria:
· Institute of Biology and Immunology of Reproduction, Bulgarian Academy of Sciences
Canada:
· Lunella Biotech. Inc.,
Chile:
· IMPACT CENTER, Universidad de Los Andes
China:
· Kunming Medical University · Shanghai jiaotong university
Czech Republic:
· Charles University and General University Hospital in Prague · Institute Of Physiology Of The Czech Acad. Sci. · Institute of Physiology, Czech Academy of Sciences
Finland:
· Tampere University · University of Eastern Finland
France:
· CEA MIRCen CNRS UMR 9199 · INSERM INM · INTERNATIONAL SPACE FEDERATION · L'Oreal R&I · Proya Europe · Université paris Cité, INSERM · University Paris-Saclay; INRAE
Germany:
· Albstadt-Sigmaringen University · Charité - Universitätsmedizin Berlin · Deutsches Herzzentrum der Charité · Deutsches Herzzentrum der Charite · Universitätsklinikum Erlangen · Dr. Mühlhausen · HAW Albstadt-Sigmaringen · Universitätsklinikum Essen · University Albstadt-Sigmaringen · University Medical Center Göttingen
Greece:
· EK PA
India:
· Indian Institute of Science Education and Research Tirupati, India · National Institute of Pharmaceutical Education and Research (NIPER) - Ahmedabad
Israel:
· Hebrew University of Jerusalem · Minovia Therapeutics Ltd. · Neurim Pharamceuticals · Sheba Medical Center
Italy:
· Crab Sinergy Srl · IDI IRCCS- Fondazione Maria Luigi Monti · Institute of Cristallography, National Council of Research · IRCCS San Raffaele Scientific Institute · National Research Council (CNR) · Polytechnic University of Marche
· Università degli Studi dell'Insubria · Università degli Studi di Bari · University of Milan · University of Padova · University of Salento · University of Turin · University of Verona
Japan:
· Hokkaido University · Kyowa Kirin · National Cerebral and Cardiovascular Center Research Institute · Tokyo University of Science
Kazakhstan:
· Nazarbayev University
Lithuania:
· Lithuanian University of Health Sciences
Luxembourg:
· University of Luxembourg
Mexico:
· Universidad de Guanajuato
Monaco:
· Biotech Investor
Netherlands:
· Amsterdam UMC · Maastricht University · Radboud University Department of Microbiology · UMC Utrecht
Norway:
· Miphic · University of Oslo
Poland:
· Adam Mickiewicz University in Poznań · Institute of Fundamental Technological Research, Polish Academy of Sciences · Nencki Institute of Experimental Biology PAS · Warsaw University of Life Sciences
· Wroclaw Medical University
Singapore:
· National University of Singapore
Slovakia:
· OVOGENE / IFG
Slovenia:
· University of Ljubljana · University of Ljubljana, Faculty of Pharmacy · University of Maribor
South Korea:
· CHA University · Institute of Endemic Diseases / Seoul National University Medical Research Center · Korea Institute of Science and Technology (KIST) School · Seoul National University College of Medicine
Spain:
· Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain · Universidad de Zaragoza
· University of Oviedo
Sweden:
· Karolinska Institutet · Stockholm Univerisity
Switzerland:
· ETH Zürich · Novartis Biomedical Research
· University of Basel
Turkey:
· Hacettepe University · Koc University · Kocaeli University, Department of Stem Cell
United Kingdom:
· Altos Labs UK · CellSpex Ltd · King’s College London · Northumbria University, Newcastle University · The Roger Williams Institute of Liver Studies · University of Bath · University of Cambridge
United States:
· Aardvark Therapeutics · ASU School of Molecular Sciences · Ciity of Hope National Medical Center · Colossal Biosciences · Labryo Fertility Center · Michael J Fox Foundation · No affiliation · Social Profit Network · Solid Biosciences · Stanford University · Throne Biotechnologies · University of California Los Angeles · University of California San Diego · University of California San Francisco (UCSF) · University of California, San Diego/ Neurosciences · University of South Dakota · UT Texas MD Anderson Cancer Center · Vertex Pharmaceuticals · Wayne State University · Wayne State University, Detroit · West Virginia University
As mitochondria move from passive subjects of research to dynamic targets for intervention, the 2025 Congress will serve as a global platform to chart the path from observation to transformation, from understanding energy to engineering health.
Discover who is attending and explore the full scientific program.
Best Image Award 2025 Winners Announced
We are thrilled to reveal the three winners of the Best Image in Mitochondria Research 2025!
Mitochondria & Organelle Crosstalk - Rethinking Organelle Crosstalk: Mitochondrial-Derived Vesicles in Peroxisome Biogenesis Presented by Dr. Ayumu Sugiura
At the heart of cellular metabolism, mitochondria and peroxisomes play tightly interconnected roles in lipid regulation, redox homeostasis, and energy dynamics. While direct contacts between these organelles have long been observed, the mechanisms underlying their communication and biological significance are only beginning to emerge.
In an insightful presentation, Dr. Ayumu Sugiura of Juntendo University, Japan, introduces a compelling hypothesis: mitochondrial-derived vesicles (MDVs) may serve as essential mediators in peroxisome biogenesis. These vesicles, generated by mitochondria in response to cellular cues, could carry lipids, enzymes, or signaling molecules critical for initiating or modulating peroxisomal function.
“Mitochondrial-derived vesicles may provide a missing mechanistic link in understanding how mitochondria influence peroxisome formation and specialization,” says Dr. Sugiura.
His talk emphasized that this vesicular communication is not a byproduct of stress or degradation but a targeted and regulated form of inter-organelle signaling, reflecting a deeper evolutionary connection.
Understanding MDVs and their role in peroxisome biology may open new avenues in treating metabolic disorders, neurodegenerative diseases, and inherited mitochondrial syndromes, where organelle cooperation is often impaired.
This new perspective encourages scientists to rethink organelle crosstalk not as static interactions but as dynamic exchanges of molecular information, and places MDVs at the center of this emerging dialogue.
Targeting Mitochondrial Pyruvate Carrier: Impact on Future Metabolic Therapies
Prof. Edmund Kunji from the University of Cambridge will give a major talk entitled Targeting mitochondrial pyruvate carrier: impact on future metabolic therapies, during the Targeting Mitochondria 2025 Congress, which will be held on October 22-24, in Berlin, Germany.
About Prof. Kunji's talk:
Fifty years after the mitochondrial pyruvate carrier (MPC) was first identified, researchers have now resolved its molecular structure and mechanism of action. In a landmark study published in Science Advances, Sichrovsky et al. (2025) unveiled how this critical mitochondrial complex mediates pyruvate transport and how its inhibition could be leveraged for therapeutic purposes in cancer, metabolic disorders, and more.
About his outstanding study:
Major Discoveries of the Study by Prof. Edmund Kunji and his teams
Molecular Structure of MPC:
The authors used cryo-electron microscopy to capture the architecture of the human MPC complex. They discovered that MPC forms a heterodimeric transport unit (MPC1/MPC2), creating a selective channel that guides pyruvate across the inner mitochondrial membrane.
Mechanism of Transport and Inhibition:
The study revealed how small-molecule inhibitors bind to the MPC complex and block its function, offering a blueprint for drug development. Structural analysis pinpointed specific binding sites that explain both transport dynamics and inhibition sensitivity.
Conserved Functionality:
Evolutionary conservation of the MPC mechanism across species (including yeast and human) underscores its universal biological role in cellular energy homeostasis.
Therapeutic Implications
Cancer:
Some tumors overexpress MPC to fuel high mitochondrial activity. MPC inhibitors could starve these cells of essential metabolites, selectively disrupting their growth.
Metabolic Diseases:
In conditions like non-alcoholic fatty liver disease (NAFLD), blocking MPC forces hepatocytes to burn fat instead of relying on glucose, leading to reduced liver fat accumulation.
Regenerative Medicine & Hair Growth:
MPC inhibition has been shown to stimulate lactate production, which may promote hair follicle cell activation, opening potential new treatments for alopecia.
Mitochondrial Dysfunction & Neurodegeneration:
Targeting MPC may allow modulation of energy metabolism in neurodegenerative and mitochondrial diseases, where ATP production and redox balance are impaired.
Broader Impact
Drug Development:
The structural elucidation of MPC provides a molecular framework for designing selective modulators, setting the stage for new classes of metabolic drugs.
Precision Medicine:
Understanding individual differences in MPC structure/function may lead to personalized metabolic therapies tailored to genetic or disease-specific metabolic profiles.
Synthetic Biology & Bioenergetics:
The detailed MPC model can inform the engineering of customized metabolic pathways, supporting advances in synthetic biology, cell therapies, and biotechnology.
Keynote Speech: Targeting Mitochondrial Channels: Update and Strategies
Keynote Speech: Targeting Mitochondrial Channels: Update and Strategies
In his keynote speech, Prof. Szewczyk will provide the latest insights into the role of mitochondrial channels in cellular function and disease. He will discuss recent advancements and strategic approaches for targeting these channels, highlighting their potential in therapeutic interventions.
About Adam Szewczyk
Adam Szewczyk is a Professor of Biochemistry and former director of the Nencki Institute of Experimental Biology (Polish Academy of Sciences) in Poland, and since 2022, he has served as the President of the Polish Biochemical Society. He completed his chemical studies at Warsaw University and his postdoctoral fellowship at Bern University (Switzerland), Institute of Cellular and Molecular Pharmacology-Nice University (France), and at Johns Hopkins University, Baltimore, MD. He is the Head of the Laboratory of Intracellular Ion Channels at Nencki Institute.
His research is focused on the role of ion channels on mitochondrial function and intracellular ion channels pharmacology and biophysical properties of mitochondrial potassium channels.
World Mitochondria Society
Annual World Congress on Targeting Mitochondria
October 22-24, 2025 - Berlin, Germany
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Development of Mitochondria-Based Therapeutic Strategies for Disease Treatment
We are pleased to announce that Prof. Kosuke Kusamori from Tokyo University of Science, Japan, will be presenting his pioneering research on "Development of Mitochondria-Based Therapeutic Strategies for Disease Treatment."
Summary
In recent years, the application of mitochondria isolated from cells for disease treatment has gained increasing attention, with their efficacy demonstrated in several diseases. However, the functions and characteristics of isolated mitochondria remain largely unknown, and their kinetics after administration into the body have yet to be fully elucidated.
Prof. Kusamori has been investigating the physical properties and in vivo kinetics of isolated mitochondria. In this talk, Prof. Kusamori will present his research on mitochondria-based therapeutic strategies aimed at advancing mitochondrial therapeutics.
World Mitochondria Society
Annual World Congress on Targeting Mitochondria
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How Mitochondria Organize Their Powerhouse Machinery for Optimal Performance
We are pleased to announce that Dr. Florent Waltz from the University of Basel, Switzerland, will be presenting at the Targeting Mitochondria 2025 congress in Berlin, Germany, on October 22-24, 2025.
Dr. Waltz will share insights from his groundbreaking research on "How Mitochondria Organize Their Powerhouse Machinery for Optimal Performance" with a special focus on photosynthetic organisms.
Key Highlights:
- In Situ Visualization: Researchers employed advanced imaging techniques to observe the mitochondrial respiratory chain within intact cells, providing a detailed view of its native architecture.
- Respiratory Supercomplexes: The study offers insights into how respiratory complexes assemble into supercomplexes, which are crucial for efficient electron transport and energy production in cells.
- Functional Implications: Understanding the organization of these supercomplexes sheds light on their role in cellular metabolism and energy conversion, potentially informing research into mitochondrial-related diseases.
Perspective:
- Challenging previous assumptions: The findings challenge long-standing models that assumed a more fluid, random distribution of respiratory chain components in mitochondrial membranes.
- Biological relevance: By analyzing structures in situ, this study underscores the importance of studying macromolecular organization in native cellular contexts, rather than relying only on purified proteins.
- Broader implications: These insights are critical not only for basic mitochondrial biology but also for understanding mitochondrial dysfunction in aging, neurodegenerative diseases, and metabolic disorders.
- New model for mitochondrial function: This study supports a model in which the geometrical and biochemical compartmentalization within cristae contributes significantly to the efficiency of oxidative phosphorylation.
These findings enhance our comprehension of mitochondrial function and may have implications for addressing metabolic disorders linked to mitochondrial dysfunction.
About the Speaker:
Dr. Florent Waltz leads research at the University of Basel focusing on mitochondrial biology and evolution in photosynthetic organisms, particularly micro-algae. His laboratory employs state-of-the-art imaging technologies to reveal the intricate details of how these essential organelles function and adapt.
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