For people living with chronic nerve pain, even a light touch can hurt. Researchers at Duke University School of Medicine say they may have found a new way to treat that pain by restoring healthy mitochondria in damaged nerves.
In a study published in Nature, the team used human tissue and mouse models to test if replenishing mitochondria could help damaged nerve cells recover. The treatment significantly reduced pain linked to diabetic neuropathy and chemotherapy-related nerve damage. In some cases, the relief lasted up to 48 hours.
The researchers said the approach may target one of the underlying causes of chronic nerve pain, instead of simply blocking pain signals, by restoring the energy supply nerve cells need to function properly.
“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.”
The findings add to evidence that cells can transfer mitochondria to one another. The Duke researchers focused on satellite glial cells, which surround and support sensory neurons.
The study found these cells appear to pass healthy mitochondria directly into sensory neurons through tiny structures called tunneling nanotubes. Ji said when this transfer process breaks down, nerve fibers begin to deteriorate.
That damage can trigger pain, tingling and numbness, especially in the hands and feet where nerve fibers extend the farthest.
“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 researchers increased this mitochondrial transfer in mice, pain-related behaviors dropped by as much as 50 percent.
The team also tested a more direct method by injecting isolated mitochondria from humans and mice into the dorsal root ganglia, clusters of nerve cells that send sensory information to the brain.
The results depended heavily on the quality of the mitochondria. Healthy donor mitochondria reduced pain, while mitochondria taken from people with diabetes produced no benefit.
Researchers also identified a protein called MYO10 as critical for creating the tunneling nanotubes that allow mitochondria to move between cells.
Ji worked with lead author Jing Xu, PhD, a research scholar in the Department of Anesthesiology, and Cagla Eroglu, PhD, a Duke professor of cell biology known for her work studying glial cells.
The researchers said more studies are needed, including high resolution imaging to better understand how the nanotubes deliver mitochondria within living nerve tissue.
The study is titled Mitochondrial transfer from glia to neurons protects against peripheral neuropathy.
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