Restoring mitochondria shows promise for treating chronic nerve pain   

(Press-News.org) For millions living with nerve pain, even a light touch can feel unbearable. Scientists have long suspected that damaged nerve cells falter because their energy factories known as mitochondria don’t function properly.

Now research published in Nature suggests a way forward: supplying healthy mitochondria to struggling nerve cells.   

Using human tissue and mouse models, researchers at Duke University School of Medicine found that replenishing mitochondria significantly reduced pain tied to diabetic neuropathy and chemotherapy-induced nerve damage. In some cases, the relief lasted up to 48 hours.   

Instead of masking symptoms, the approach could fix what the team sees as the root problem — restoring the energy flow that keeps nerve cells healthy and resilient.

“By giving damaged nerves fresh mitochondria — or helping them make more of their own — we can reduce inflammation and support healing,” said the study’s senior author Ru-Rong Ji, PhD, director of the Center for Translational Pain Medicine in the Department of Anesthesiology at Duke School of Medicine. “This approach has the potential to ease pain in a completely new way.”   

Their findings build on growing evidence that cells can swap mitochondria, a process that scientists are beginning to recognize as a built-in support system that may affect many conditions including obesity, cancer, stroke, and chronic pain.

The secret life of glial cells

The work highlights a previously undocumented role for satellite glial cells, which appear to deliver mitochondria to sensory neurons through tiny channels called tunnelling nanotubes.

When this mitochondrial handoff is disrupted, Ji said, nerve fibers begin to degenerate — triggering pain, tingling and numbness, often in the hands and feet, the distal ends of the nerve fibers.

"By sharing energy reserves, satellite glial cells may help keep neurons out of pain," said Ji, a professor of anesthesiology, neurobiology and cell biology at Duke School of Medicine. 

When this energy transfer was boosted, pain behaviors in mice dropped by as much as 50%, the study showed.

Researchers also tried a more direct approach. Injecting isolated mitochondria whether from humans or mice directly into the dorsal root ganglia, a cluster of nerve cells that send messages to the brain, produced similar results, but only when the donor mitochondria were healthy; samples from people with diabetes had no effect.

The team also identified a protein, MYO10, as essential for forming the nanotubes that enable the mitochondrial transfer.

Ji, worked with lead author Jing Xu, PhD, a research scholar in the Department of Anesthesiology, along with longtime collaborator Caglu Eroglu, PhD, a Duke professor of cell biology known for her expertise in glial cell behavior.

More work is needed, including high-resolution imaging to confirm precisely how nanotubes help deliver fresh mitochondria in living nerve tissue.

Even so, the study highlights a previously overlooked communication pathway between nerve and glial cells that could treat chronic pain at its source.

 

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