Duke University researchers report that boosting the transfer of healthy mitochondria from support cells to sensory neurons reduced pain-like behaviors in mouse models of diabetic and chemotherapy-related peripheral neuropathy, an approach they say could address a root driver of nerve pain rather than simply blocking pain signals.
Researchers at Duke University School of Medicine say they have identified a cell-to-cell “recharging” process that may help explain — and potentially counter — chronic nerve pain caused by peripheral neuropathy.
In a study published in Nature, the team used experiments in human tissue and mouse models to examine how satellite glial cells, which surround sensory neurons in the dorsal root ganglia, deliver mitochondria — the cell’s energy-producing structures — into nearby neurons through tunneling nanotube-like structures. The researchers reported that neuropathy-linked conditions disrupted this transfer and that restoring or enhancing it reduced pain-related behaviors in mice.
When the researchers increased mitochondrial transfer in mice, pain-related behaviors fell by as much as 50%, Duke said in a summary of the findings. In some experiments, the pain relief lasted up to 48 hours.
The Duke report also said the team tested a more direct approach by injecting isolated mitochondria into dorsal root ganglia, finding that outcomes depended on mitochondrial health: mitochondria from healthy donors reduced pain in mice, while mitochondria from people with diabetes did not. The researchers additionally identified the protein MYO10 as important for forming the tunneling nanotubes that enable the transfer.
The work remains preclinical, and the researchers said further studies are needed to clarify exactly how the nanotube structures deliver mitochondria in living nerve tissue and to assess whether the strategy could translate into treatments for people with chronic neuropathic pain.
