A (heat) shock to the system promotes peripheral nerve regeneration
Ahmet Höke
Ahmet Höke
Published November 1, 2011; First published October 3, 2011
Citation Information: J Clin Invest. 2011;121(11):4231-4234. https://doi.org/10.1172/JCI59320.
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Commentary

A (heat) shock to the system promotes peripheral nerve regeneration

Abstract

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.

Authors

Ahmet Höke

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Figure 1

Challenges to successful regeneration with proximal injuries.

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Challenges to successful regeneration with proximal injuries. Good senso...
Good sensory and motor recovery is likely if surgery is not delayed after a distal nerve injury, such as median nerve injury at the carpal tunnel. However, motor recovery after a more proximal injury, for example, to the ulnar nerve at the cubital tunnel in the elbow, is likely to be slow and incomplete due to the atrophic changes that take place in the distal portions of the nerve. One of the key reasons for this poor recovery of motor function is the slow rate of axonal regeneration; it takes too long for the injured axons to regenerate and connect with Schwann cells and muscle.