粒体自噬
疾病
糖尿病
胰岛素抵抗
医学
氧化应激
自噬
线粒体
生物信息学
神经科学
生物
内分泌学
细胞生物学
病理
细胞凋亡
遗传学
作者
Kiavash Hushmandi,Behzad Einollahi,Rachel Aow,Suhana Binte Suhairi,Daniel J. Klionsky,Amir Reza Aref,Rüssel J. Reiter,Pooyan Makvandi,Navid Rabiee,Yi Xu,Noushin Nabavi,Seyed Hassan Saadat,Najmeh Farahani,Alan Prem Kumar
标识
DOI:10.1016/j.phrs.2024.107394
摘要
Mitophagy, the cellular process of selectively eliminating damaged mitochondria, plays a crucial role in maintaining metabolic balance and preventing insulin resistance, both key factors in type 2 diabetes mellitus (T2DM) development. When mitophagy malfunctions in diabetic neuropathy, it triggers a cascade of metabolic disruptions, including reduced energy production, increased oxidative stress, and cell death, ultimately leading to various complications. Thus, targeting mitophagy to enhance the process may have emerged as a promising therapeutic strategy for T2DM and its complications. Notably, plant-derived compounds with β-cell protective and mitophagy-stimulating properties offer potential as novel therapeutic agents. This review highlights the intricate mechanisms linking mitophagy dysfunction to T2DM and its complications, particularly neuropathy, elucidating potential therapeutic interventions for this debilitating disease.
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