Xing QC, Chen J, Liu Z, Li WC, Liu X, Li W. Autophagy in Schwann cells: A potential pharmacotherapeutic target in diabetic peripheral neuropathy. World J Diabetes 2025; 16(6): 105709 [DOI: 10.4239/wjd.v16.i6.105709]
Corresponding Author of This Article
Qi-Chang Xing, Assistant Professor, Department of Clinical Pharmacy, Xiangtan Central Hospital (The Affiliated Hospital of Hunan University), No. 120 Heping Road, Xiangtan 411100, Hunan Province, China. 67324457@qq.com
Research Domain of This Article
Endocrinology & Metabolism
Article-Type of This Article
Minireviews
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Qi-Chang Xing, Jia Chen, Zheng Liu, Wen-Can Li, Xiang Liu, Wei Li, Department of Clinical Pharmacy, Xiangtan Central Hospital (The Affiliated Hospital of Hunan University), Xiangtan 411100, Hunan Province, China
Co-corresponding authors: Qi-Chang Xing and Wei Li.
Author contributions: Xing QC and Li W conceptualized and designed the study, created the artwork, supervised, and made critical revisions, they contributed equally as co-corresponding authors; Liu Z, Li WC, and Liu X conducted the literature review, performed the analysis, interpretated the data, and drafted the original manuscript; Xing QC, Chen J, Liu Z, Li WC, Liu X, and Li W prepared the draft and approved the submitted version.
Supported by Natural Science Foundation of Hunan Province, No. 2023JJ60497; Chinese Medicine Research Program of Hunan Province, No. 2021169; and Xiangtan Medical Research Project Plan, No. 2022-xtyx-34 and No. 2022-xtyx-36.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Qi-Chang Xing, Assistant Professor, Department of Clinical Pharmacy, Xiangtan Central Hospital (The Affiliated Hospital of Hunan University), No. 120 Heping Road, Xiangtan 411100, Hunan Province, China. 67324457@qq.com
Received: February 5, 2025 Revised: March 27, 2025 Accepted: May 16, 2025 Published online: June 15, 2025 Processing time: 129 Days and 10.9 Hours
Abstract
Diabetic peripheral neuropathy (DPN) is a common complication of diabetes and is characterized by sensory and motor impairments resulting from neural injury. Schwann cells (SCs), which are important for peripheral nerve function, are compromised under hyperglycemic conditions, leading to impaired axonal regeneration and demyelination. Autophagy, a cellular degradation process, is essential for SC function and significantly influences DPN progression. This article highlights the significance of autophagy in SCs and its potential as a pharmacotherapeutic target in DPN. We discuss the mechanisms of autophagy in SCs, including the mammalian target of rapamycin, adenosine monophosphate-activated protein kinase, and phosphatase and tensin homolog-induced putative kinase/parkin pathways, and their dysregulation in DPN. This article also examines various natural products and chemical agents that modulate autophagy and enhance the efficacy of DPN treatment. These agents target key signaling pathways, such as adenosine monophosphate-activated protein kinase/mammalian target of rapamycin and demonstrate potential in promoting nerve regeneration and restoring SC function. The roles of exosomes, long non-coding RNA, and proteins in the regulation of autophagy have also been explored. In conclusion, targeting autophagy in SCs is a promising strategy for DPN treatment and offers new insights into therapeutic interventions. Further research is warranted to fully exploit these targets for clinical applications.
Core Tip: This article underscores the critical role of autophagy in Schwann cells in the progression of diabetic peripheral neuropathy progression, highlight its potential as a pharmacotherapeutic target. It explored autophagy mechanisms (mammalian target of rapamycin, adenosine monophosphate-activated protein kinase, and phosphatase and tensin homolog-induced putative kinase/parkin pathways), their dysregulation in diabetic peripheral neuropathy, and various autophagy-modulating agents (natural products and chemical drugs) that promote nerve regeneration and recovery of Schwann cell function.
