周围神经损伤
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Figure 1｜Flow chart of article retrieval.
Data retrieval is shown in Figure 1.
Figure 2｜PNI repair mechanism.
After an injury, the distal nerve stump undergoes Wallerian degeneration, in which the nerve fiber (distal stump) degenerates. Markers related to myelin formation are downregulated, and Schwann cells change to a repair phenotype that bears a resemblance to the immature form as shown in Figure 2A (Jessen and Mirsky, 2016; Carr and Johnston, 2017; Welleford et al., 2020; Wilcox et al., 2020). Schwann cells with a repair phenotype cast off their myelin, acquire mobility and secrete neurotrophic factors like NGF, BDNF, NT-3, and GDNF to promote axon regeneration (H?ke et al., 2006; Xu et al., 2013; Park and H?ke, 2014; Jessen and Mirsky, 2016; Figure 2A). An outstanding study by Welleford et al. (2020) used RNA sequencing to properly analyze the human peripheral nerve’s whole transcriptome profile following injury. The researchers discovered 3641 genes that were significantly differentially expressed, the majority related to growth factor upregulation, most noticeably GDNF (Welleford et al., 2020).
Macrophages, neutrophils, and the reprogrammed Schwann cells breakdown myelin debris and clear the injured axonal membrane and cytoskeleton as seen in Figure 2B (Tomlinson et al., 2018). Additionally, Schwann cells associate with fibroblasts to synthesize adhesion proteins and extracellular matrix, allowing for successful bridging between proximal and distal stumps (review by Jessen and Mirsky, 2016; Figure 2B). Schwann cells align at the distal stump, forming bands of Büngner to provide trophic and physical support and direct axonal regeneration (Figure 2B). Once axonal regeneration has concluded, Schwann cells differentiate to their mature phenotype and re-myelinate the axons as reviewed by Boerboom et al. (2017; Figure 2C).