Cellular mitochondria transfer prevents pain

January 27, 2026

Cellular mitochondria transfer prevents pain

Cellular structures called mitochondria provide sensory neurons with the energy they need to send signals to the brain. Cancer chemotherapy drugs and diabetes can damage mitochondria in those cells, leading to a kind of nerve damage called peripheral neuropathy. This condition causes pain and weakness, typically in the hands and feet.

An NIH-funded research team led by Dr. Ru-Rong Ji of Duke University Medical Center sought new ways to treat peripheral neuropathy by studying how sensory neurons in mice maintain their supply of mitochondria. The research was published on January 7, 2026, in the journal Nature.

The team's experiments focused on clusters of sensory neurons located near the spinal cord known as dorsal root ganglia (DRG). Neurons in the DRG have supporting cells wrapped around them called satellite glial cells (SGCs).

The researchers found that mitochondria can move from mouse SGCs to DRG sensory neurons via connecting structures called tunnelling nanotubes. This transfer occurred in both cultured mouse cells and in live mice. Disrupting nanotube formation blocked the mitochondrial transfer.

Treating mice with a chemotherapy drug, paclitaxel, impaired nanotube formation. Also, mitochondrial movement from SGCs to DRG neurons was reduced in a mouse model of diabetic nerve damage.

Prior studies had found a molecular motor protein called myosin 10 (MYO10) in nanotubes. The team found high levels of MYO10 in healthy mouse SGCs. MYO10 was also found in the nanotubes connecting SGCs to DRG neurons.

Reducing MYO10 levels in living mice reduced nanotube formation and inhibited the transfer of mitochondria from SGCs to DRG neurons in cultured cells and live mice. Mice with reduced levels of MYO10 were also more sensitive to pain.

The researchers observed mitochondrial transfer from SGCs to neurons in DRG from human donors. SGCs from healthy people had high levels of MYO10 gene activity. But in SGCs from people with diabetes, MYO10 activity was lower. Also, tunnelling nanotubes connecting the SGCs and DRG neurons of people with diabetes had structural abnormalities that restricted mitochondrial transfer.

Injecting SGCs from healthy human donors into the spinal DRGs of diabetic mice reduced their sensitivity to pain. Injections of SGCs from healthy mice into mice treated with paclitaxel similarly reduced pain sensitivity. This pain-relieving effect required MYO10, as SGCs with reduced MYO10 levels did not improve pain sensitivity.

The team also tried isolating mitochondria from human SGCs and injecting them into DRGs of diabetic or paclitaxel-treated mice. Mitochondria from healthy human donors decreased pain sensitivity in both groups of mice. But mitochondria from human donors with diabetes did not.

The results suggest a previously unrecognized role for SGCs in protecting against peripheral neuropathy by transferring their mitochondria to neurons. This transfer occurs via tunnelling nanotubes whose formation requires MYO10. Chemotherapy and diabetes can cause peripheral neuropathy by disrupting this process. The findings also suggest a strategy for treating neuropathic pain by transferring healthy SGCs or their mitochondria.

"By giving damaged nerves fresh mitochondria-or helping them make more of their own-we can reduce inflammation and support healing," Ji says. "This approach has the potential to ease pain in a completely new way."

Related Links

• Non-opioid compound for chronic pain relief
• Characterizing what human sensory nerves can sense
• Cancer cells drain energy from immune cells
• Managing pain
• Peripheral neuropathy
• Diabetic neuropathy
• Chemotherapy to treat cancer

References

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.

Funding

NIH's National Institute of Neurological Disorders and Stroke (NINDS); Department of Defense; Duke University; Paul and Daisy Soros Fellowships for New Americans; Howard Hughes Medical Institute; Michael J. Fox Foundation; Aligning Science Across Parkinson's.