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高血糖诱导糖尿病周围神经病变中施万细胞凋亡。

Schwann cells apoptosis is induced by high glucose in diabetic peripheral neuropathy.

机构信息

Department of Anatomy, School of Basic Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.

Department of Anatomy, School of Basic Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.

出版信息

Life Sci. 2020 May 1;248:117459. doi: 10.1016/j.lfs.2020.117459. Epub 2020 Feb 21.

DOI:10.1016/j.lfs.2020.117459
PMID:32092332
Abstract

Diabetic peripheral neuropathy (DPN) is a common complication of diabetes mellitus that affects approximately half of patients with diabetes. Current treatment regimens cannot treat DPN effectively. Schwann cells (SCs) are very sensitive to glucose concentration and insulin, and closely associated with the occurrence and development of type 1 diabetic mellitus (T1DM) and DPN. Apoptosis of SCs is induced by hyperglycemia and is involved in the pathogenesis of DPN. This review considers the pathological processes of SCs apoptosis under high glucose, which include the following: oxidative stress, inflammatory reactions, endoplasmic reticulum stress, autophagy, nitrification and signaling pathways (PI3K/AKT, ERK, PERK/Nrf2, and Wnt/β-catenin). The clarification of mechanisms underlying SCs apoptosis induced by high glucose will help us to understand and identify more effective strategies for the treatment of T1DM DPN.

摘要

糖尿病周围神经病变(DPN)是糖尿病的一种常见并发症,约影响一半的糖尿病患者。目前的治疗方案无法有效治疗 DPN。许旺细胞(SCs)对葡萄糖浓度和胰岛素非常敏感,与 1 型糖尿病(T1DM)和 DPN 的发生和发展密切相关。高血糖诱导 SCs 凋亡,并参与 DPN 的发病机制。本综述考虑了高葡萄糖下 SCs 凋亡的病理过程,包括以下几个方面:氧化应激、炎症反应、内质网应激、自噬、硝化和信号通路(PI3K/AKT、ERK、PERK/Nrf2 和 Wnt/β-catenin)。阐明高葡萄糖诱导 SCs 凋亡的机制将有助于我们理解和确定更有效的 T1DM DPN 治疗策略。

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