Researchers at Duke University report that mitochondria transfer to damaged nerve cells reduces chronic nerve pain in human tissue and mice, offering a potential new treatment for diabetic neuropathy and chemotherapy-related nerve damage.
Scientists say the findings, published this week in the journal Nature, point to a way to treat pain by repairing the underlying energy failure inside nerve cells rather than masking symptoms.
Chronic nerve pain affects millions worldwide and can make even light touch feel severe. Previous research has linked the condition to malfunctioning mitochondria, the structures that produce energy within cells.
Healthy Mitochondria Reduce Pain in Tests
Using human nerve tissue and mouse models, Duke University School of Medicine researchers found that mitochondria transfer to damaged nerve cells significantly reduced pain behaviors associated with diabetic neuropathy and chemotherapy-induced nerve injury.
In some experiments, pain relief lasted up to 48 hours. In mice, pain-related behaviors dropped by as much as 50%, according to the study.
“By giving damaged nerves fresh mitochondria, or helping them produce more of their own, we can reduce inflammation and support healing,” said Ru-Rong Ji, Ph.D., the study’s senior author and director of the Center for Translational Pain Medicine at Duke. “This approach treats pain in a completely different way.”
Researchers injected isolated mitochondria directly into the dorsal root ganglia, clusters of nerve cells that relay signals to the brain. The treatment worked only when the mitochondria came from healthy donors. Mitochondria taken from people with diabetes had no effect.
Glial Cells Play Key Support Role
The study also identifies a previously undocumented role for satellite glial cells, which support sensory neurons. The researchers found that these cells facilitate mitochondria transfer to neurons through tiny structures called tunneling nanotubes.
When this transfer was blocked, nerve fibers began to degenerate, triggering pain, tingling and numbness, particularly in the hands and feet.
“Satellite glial cells appear to act as energy suppliers,” Ji said. “By sharing energy reserves, they may help keep neurons functioning and out of pain.”
The team identified a protein known as MYO10 as essential for forming the nanotubes that enable mitochondria transfer between cells. Disrupting this protein blocked the process and worsened nerve damage in mice.
Jing Xu, Ph.D., the study’s lead author and a research scholar at Duke, said the findings highlight how closely nerve cells depend on their neighboring support cells.
“This communication pathway was largely overlooked,” Xu said. “Understanding it gives us a new target for treating chronic pain.”
Path Toward New Pain Treatments
The research builds on growing evidence that cells can exchange mitochondria as part of a natural support system. Scientists believe this process may influence a range of conditions, including obesity, cancer, stroke and chronic pain.
Caglu Eroglu, Ph.D., a Duke professor of cell biology and a co-author of the study, said the work changes how scientists view glial cells.
“They are not just passive support cells,” Eroglu said. “They actively help maintain neuron health.”
The researchers caution that more work is needed before the approach can be tested in people. Future studies will use high-resolution imaging to confirm how mitochondria transfer occurs in living nerve tissue and to evaluate long-term safety.
Still, the findings suggest a strategy that targets the root cause of nerve pain by restoring energy flow inside damaged cells.
“If we can keep nerve cells healthy and resilient,” Ji said, “we may be able to prevent chronic pain from developing in the first place.”
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