Protein identified as brake on nerve regeneration
Mount Sinai researchers discovered that the aryl hydrocarbon receptor (AHR) suppresses axon regrowth after nerve injury. Blocking AHR in mice allowed damaged nerve fibers to regrow and improved movement and sensation. The findings, published in Nature, could lead to new treatments that promote nerve repair.
AHR was originally characterized as a sensor for environmental toxins and pollutants, a class of compounds known as xenobiotics. This new research reveals a broader biological function: within neurons, the protein appears to link external environmental cues to internal decisions about whether a damaged cell prioritizes stress management or active reconstruction of its connections.
The study, published in Nature, used mouse models of both peripheral nerve damage and spinal cord injury. When AHR was genetically removed or pharmacologically blocked, injured axons regenerated more successfully, and the animals showed improved movement and sensation. The regenerative response depended on HIF-1α, a factor that regulates genes tied to metabolism and tissue repair.
These findings could eventually inform treatments for people with peripheral nerve injuries or spinal cord damage, conditions that often cause lasting impairment of movement and sensation. If therapies targeting AHR prove safe and effective in humans, they may shift recovery outcomes for patients who currently face limited regenerative options. However, clinical application remains distant, and the balance between suppressing stress responses and promoting repair will require careful study.