Scientists Discover New Way To Reduce Chronic Nerve Pain By Repairing Cells

Millions of people live with chronic nerve pain that can turn even a light touch into severe discomfort and disrupt everyday life. A growing body of research suggests that this pain often begins when mitochondria — the tiny energy-producing structures inside cells — stop functioning properly in damaged nerves.

Researchers at Duke University School of Medicine now report that restoring healthy mitochondria in nerve cells could open a new direction for treating chronic neuropathic pain. Their findings, published in Nature in May 2024, point toward an approach aimed at repairing damaged nerves rather than simply blocking pain signals.

The Duke team studied both human tissue and mouse models of painful nerve damage, including diabetic neuropathy and chemotherapy-induced neuropathy. They discovered that replenishing or strengthening healthy mitochondria in sensory nerves significantly reduced pain-related behaviors in animals.

In some experiments, a single treatment provided relief for up to 48 hours. Unlike traditional pain medications that mainly target receptors or nerve activity, this strategy appears to restore cellular energy production and improve the overall health of damaged neurons, potentially addressing one of the underlying causes of chronic pain.

Senior author Ru-Rong Ji, director of the Center for Translational Pain Medicine at Duke, explained that supplying fresh mitochondria or helping nerves produce more of their own may reduce inflammation and support nerve recovery. The study builds on earlier research linking mitochondrial dysfunction to chronic pain and neurodegenerative diseases.

Support Cells Transfer Healthy Mitochondria

The researchers focused on satellite glial cells, specialized support cells that surround sensory neurons in structures known as dorsal root ganglia. Their experiments showed that these glial cells can transfer healthy mitochondria directly into neurons through tiny cellular bridges called tunneling nanotubes.

When this mitochondrial transfer system becomes impaired, nerve fibers begin to deteriorate, contributing to symptoms such as burning pain, tingling, and numbness, especially in the hands and feet. By enhancing mitochondrial transfer between glial cells and neurons in mice, researchers observed pain-related behaviors decrease by up to 50 percent.

The findings strengthen the idea that mitochondrial transfer acts as a natural rescue mechanism within the nervous system. Similar processes have previously been observed in the brain, where support cells known as astrocytes donate mitochondria to injured neurons after strokes or other forms of damage.

A Key Protein Linked To Nerve Protection

The team also tested a more direct method by injecting isolated mitochondria from humans and mice into the dorsal root ganglia. The effectiveness of this approach depended heavily on the quality of the donor mitochondria.

Healthy mitochondria reduced pain symptoms, while mitochondria taken from people with diabetes produced little meaningful benefit. This suggests that mitochondrial health itself plays a critical role in determining treatment success.

Researchers identified a motor protein called MYO10 as essential for forming the tunneling nanotubes responsible for mitochondrial transfer between cells. When MYO10 activity was disrupted, mitochondrial transfer declined and nerve damage worsened, indicating that this pathway could become an important future therapeutic target.

The project involved collaboration between experts in anesthesiology, neurobiology, and cell biology, including glial cell researcher Cagla Eroglu and lead author Jing Xu. The findings contribute to a broader shift in pain research toward understanding how support cells and cellular metabolism influence nerve function.

What The Findings Could Mean For Future Treatments

Current treatments for chronic neuropathic pain — including antidepressants, anticonvulsants, and opioids — often provide only partial relief and may cause significant side effects. A therapy focused on restoring mitochondrial function in nerves could eventually complement or replace some symptom-based treatments.

However, researchers caution that the work remains at an early stage. Safely delivering mitochondria into human nerves, maintaining long-term effectiveness, and avoiding immune-related complications remain major scientific challenges that require extensive testing.

Scientists are now exploring improved imaging technologies to observe tunneling nanotubes and mitochondrial transfer in living tissue, along with small molecules and gene therapies that may strengthen the body’s natural repair systems.

If successful, these approaches could eventually benefit people suffering from diabetic neuropathy, chemotherapy-related nerve damage, post-surgical nerve pain, and other difficult-to-treat chronic pain conditions.

The findings also highlight the close relationship between metabolic health and nerve health. Conditions such as diabetes can damage mitochondria throughout the body, increasing the risk of nerve dysfunction and chronic pain.

While clinical applications are still likely years away, the study offers a promising glimpse into how targeting the body’s cellular energy systems could reshape the future of chronic pain treatment.