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. 2023 Feb 24;14:1081458. doi: 10.3389/fneur.2023.1081458

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Copyright © 2023 Ni, Yao, Zhao, Zhang, Wang, Li and Chen.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Mechanistic pathways of ES in the treatment of PNI. brain-derived neurotrophic factor, BDNF; Tyrosine kinase receptor, Trk; mitogen-activated proteinkinase kinase 1/2, MEK 1/2; P38 mitogen activated protein kinase, P38 MAPK; phosphoinositide 3-Kinase, PI3K; protein Kinase B, PKB(AKT); adenosine triphosphate, ATP; cyclic adenosine monophosphate, cAMP; protein kinase A, PKA; cAMP-response element binding protein, CREB; glial cell line-derived neurotrophic factor, GDNF; nerve growth factor, NGF; growth associated protein-43, GAP-43. See the text in the section “4.1.4 Mechanism” for a detailed description.