粒体自噬
自噬
线粒体
氧化应激
生物
2型糖尿病
糖尿病
细胞生物学
生物信息学
医学
内分泌学
遗传学
细胞凋亡
作者
Nadezda Apostolova,Teresa Vezza,Jordi Muntané,Milagros Rocha,Víctor M. Víctor
标识
DOI:10.1089/ars.2022.0016
摘要
Significance: Type 2 diabetes mellitus, which is related to oxidative stress and mitochondrial dysfunction, is one of the most prevalent diseases in the world. In the past decade, alterations in autophagy have been shown to play a fundamental role in the development and control of type 2 diabetes. Further, mitophagy has been recognized as a key player in eliminating dysfunctional mitochondria in this disease. Recent Advances: Recently, much progress has been made in understanding the molecular events associated with oxidative stress, mitochondrial dysfunction, and alterations in autophagy and mitophagy in type 2 diabetes. Critical Issues: Despite increasing evidence of a relationship between mitochondrial dysfunction, oxidative stress, and alterations of autophagy and mitophagy and their role in the pathophysiolology of type 2 diabetes, effective therapeutic strategies to combat the disease through targeting mitochondria, autophagy, and mitophagy are yet to be implemented. Future Directions: This review provides a wide perspective of the existing literature concerning the complicated interplay between autophagy, mitophagy, and mitochondrial dysfunction in type 2 diabetes. Further, potential therapeutic targets based on these molecular mechanisms are explored. Antioxid. Redox Signal. 39, 278-320.
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