Autophagy and Peripheral Nerve Regeneration: A Complex Relationship in Oral and Maxillofacial Regions

However, conflicting conclusions have been drawn from various studies. For instance, Roberts et al. [145] found no significant difference in nerve regeneration between mice with inhibited autophagy and control mice. Conversely, Myers' study indicated that inhibiting autophagy via p38 MAP kinase activity modulation could promote axon regeneration and myelination [146]. These inconsistent results may be attributed to injured tissue fragments blocking the pathway of axon growth, thereby hindering the regeneration of peripheral nerve fibers. Additionally, autophagy-related genes, such as c-Jun, XBP1, and C/EBP, are involved in the dedifferentiation process of Schwann cells, and inhibiting autophagy may shift the proliferation mode of Schwann cells [147-150]. Moreover, during Waller degeneration caused by Schwann cell autophagy, an increase in neurotrophic factors and ECM proteins affects the regeneration of peripheral nerves [151-153].

In summary, autophagy plays a role in peripheral nerve regeneration in the oral and maxillofacial regions. However, the research on the role of autophagy in oral and maxillofacial peripheral nerve regeneration is still limited, with most studies utilizing the sciatic nerve crush injury model in rats. Furthermore, the clinical application of autophagy in promoting nerve regeneration has not yet been realized, indicating the need for further investigation.