胰腺β细胞自噬失调与2型糖尿病的风险

Autophagy Pub Date : 2024-11-01 Epub Date: 2024-06-18 DOI:10.1080/15548627.2024.2367356
Hayder M Al-Kuraishy, Majid S Jabir, Ali I Al-Gareeb, Daniel J Klionsky, Ali K Albuhadily
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引用次数: 0

摘要

自噬是一种重要的降解过程,可清除异常细胞成分,维持细胞内的平衡,并在饥饿时提供营养。激活自噬可提高细胞在压力条件下的存活率,但过度激活自噬会诱导自噬细胞死亡。因此,早期发生的自噬可促进细胞存活,而晚期发生的自噬会导致细胞程序性死亡,从而阻止不同疾病的进展。此外,自噬通过不同的机制调节胰腺β细胞的功能,但自噬在2型糖尿病(T2D)中的确切作用尚不完全清楚。因此,这篇微型综述讨论了自噬在胰腺β细胞和T2D病理生理学中的保护和有害作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Dysregulation of pancreatic β-cell autophagy and the risk of type 2 diabetes.

Macroautophagy/autophagy is an essential degradation process that removes abnormal cellular components, maintains homeostasis within cells, and provides nutrition during starvation. Activated autophagy enhances cell survival during stressful conditions, although overactivation of autophagy triggers induction of autophagic cell death. Therefore, early-onset autophagy promotes cell survival whereas late-onset autophagy provokes programmed cell death, which can prevent disease progression. Moreover, autophagy regulates pancreatic β-cell functions by different mechanisms, although the precise role of autophagy in type 2 diabetes (T2D) is not completely understood. Consequently, this mini-review discusses the protective and harmful roles of autophagy in the pancreatic β cell and in the pathophysiology of T2D.

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