Restoring Mitochondria May Offer a New Way to Treat Chronic Nerve Pain, Study Suggests

Scientists at Duke University have identified a potential new strategy for treating chronic nerve pain by restoring the tiny energy-producing structures inside damaged nerve cells. The approach targets mitochondria—the organelles responsible for generating the energy that nerves need to function properly and repair themselves.

In a study published in Nature, the researchers found that replenishing healthy mitochondria in damaged nerves reduced pain in mouse models. The treatment alleviated neuropathic pain associated with diabetic neuropathy and chemotherapy-induced nerve damage, with pain relief lasting up to 48 hours in some experiments.

How Restoring Mitochondria Reduced Pain

Chronic neuropathic pain often develops when damaged nerves can no longer maintain adequate energy production. As mitochondrial function declines, nerve fibers become increasingly vulnerable to degeneration, leading to symptoms such as burning pain, tingling, numbness, and heightened sensitivity, particularly in the hands and feet.

Rather than simply blocking pain signals, the Duke researchers focused on improving the metabolic health of injured nerves. By restoring mitochondrial function, the treatment appeared to support nerve metabolism, reduce inflammation, and promote recovery of damaged nerve cells instead of merely relieving symptoms.

Support Cells Can Transfer Healthy Mitochondria

The researchers focused on satellite glial cells, specialized support cells that surround sensory neurons within structures known as dorsal root ganglia. They discovered that these glial cells can transfer healthy mitochondria directly to neighboring neurons.

This transfer occurs through microscopic structures called tunneling nanotubes, which create temporary connections between cells. According to the study, efficient mitochondrial transfer helped stabilize damaged nerve fibers and reduced pain-related behaviors in animal models by as much as 50%.

When this transfer process was impaired, neurons received less metabolic support, making them more vulnerable to damage. The researchers suggest that disrupted mitochondrial transfer may contribute to neuropathic pain associated with conditions such as diabetes and chemotherapy-induced nerve injury.

A Protein That Enables Mitochondrial Transfer

The team also identified an important protein called MYO10, which appears to play a key role in forming the tunneling nanotubes required for mitochondrial transport between cells. When MYO10 function was experimentally disrupted, fewer nanotubes formed, mitochondrial transfer declined, and nerve health deteriorated.

In a separate experiment, the researchers injected isolated mitochondria obtained from both human and mouse donors directly into the dorsal root ganglia of mice. Mitochondria from healthy donors reduced pain-related behaviors, whereas mitochondria obtained from people with diabetes provided little measurable benefit.

Potential for Future Pain Treatments

The findings suggest that therapies designed to enhance mitochondrial transfer—or directly deliver healthy mitochondria to damaged nerves—could represent a new approach to treating chronic neuropathic pain. Unlike many currently available medications, which primarily reduce pain signaling, these strategies aim to address one of the underlying biological processes contributing to nerve dysfunction.

The researchers emphasize, however, that the work remains at an early preclinical stage. Most of the experiments were performed in mice, and translating this approach into human treatment will require significant advances in safety, delivery techniques, and long-term evaluation before clinical use becomes possible.

Future research will focus on improving imaging of tunneling nanotubes, refining methods for mitochondrial delivery, and investigating medications capable of enhancing MYO10 activity or related biological pathways. If these approaches prove safe and effective, they may eventually offer new treatment options for people whose chronic nerve pain does not respond adequately to existing therapies.

Neuropathic pain affects millions of people worldwide and often remains difficult to manage despite currently available medications. According to the researchers, therapies that restore the energy-producing capacity of damaged nerves, rather than simply suppressing pain signals, could eventually provide a fundamentally different strategy for improving symptoms and quality of life.