Peripheral nervous system injury (PNI) is common and challenging to repair. While the peripheral nervous system (PNS) has better repair abilities than the central nervous system (CNS), it still takes a long time for complete recovery (Oblinger and Lasek, 1984). SCs, a kind of peripheral nerve glial cells, play a crucial role in PNS myelination. During nerve injury repair, SCs can convert to the repair phenotype, which is a class of transiently present intermediates that affect the repair. The temporal and quantitative stability of these cells' existence is therefore critical (Jessen and Arthur-Farraj, 2019). After nerve injury, sphingomyelin and axonal fragments accumulate in the nerve break gap. To solve this, repair Schwann cells promote the formation of inflammatory reactions (Meyer zu Hörste et al., 2010), and cooperate with macrophages to remove fragments and constantly release neurotrophic factors, providing a suitable regenerative microenvironment for nerves.

The main links of self-nerve repair include Wallerian degeneration, axon regeneration, and remyelination; especially, angiogenesis and inflammatory regulation are the critical links in the repair. When the damage is too severe or the repair is inhibited by some problems, such as a few nutritional factors and excessive inhibitory factors, artificially implanted stem cells can be used to promote the repair process (Zhang et al., 2019). Clinical trials and research have proved transplantation of SCs is practical and feasible in treating nerve injury. However, there are still many difficulties, such as the limited source of autologous nerve transplantation and the problematic survival of SCs after transplantation. Therefore, it is essential to understand the specific mechanisms and changes in the repair to find solutions to these problems.