Peripheral nerves are easily damaged, resulting in loss of motor and sensory function. Recovery of motor and sensory function after peripheral nerve injury is suboptimal, even after appropriate surgical repair. This is due to the slow rate of axonal elongation during regeneration and atrophic changes that occur in denervated Schwann cells and target muscle with proximal lesions. One way to solve this problem is to accelerate the rate at which the axons regenerate. In this issue of the JCI, Ma and colleagues show that this can be achieved in mice by overexpression of heat shock protein 27, providing hope for enhanced functional recovery in patients after peripheral nerve damage.
