粒体自噬
生物
线粒体
功能(生物学)
细胞生物学
自噬
疾病
计算生物学
机制(生物学)
神经科学
模式生物
发病机制
双重角色
生物信息学
人类疾病
受体
帕金
表型
品脱1
信号转导
作者
Qi Wang,Yu Sun,Terytty Yang Li,Johan Auwerx
出处
期刊:Cell Research
[Springer Nature]
日期:2026-01-05
卷期号:36 (1): 11-37
被引量:3
标识
DOI:10.1038/s41422-025-01203-7
摘要
Mitophagy, an evolutionarily conserved quality-control process, selectively removes damaged mitochondria to maintain cellular homeostasis. Recent advances in our understanding of the molecular machinery underlying mitophagy - from receptors and stress-responsive triggers to lysosomal degradation - illustrate its key role in maintaining mitochondrial integrity and adapting mitochondrial function to ever-changing physiological demands. In this review, we outline the fundamental mechanisms of mitophagy and discuss how dysregulation of this pathway disrupts mitochondrial function and metabolic balance, driving a wide range of disorders, including neurodegenerative, cardiovascular, metabolic, and immune-related diseases, as well as cancer. We explore the dual role of mitophagy as both a disease driver and a therapeutic target, highlighting the efforts and challenges of translating mechanistic insights into precision therapies. Targeting mitophagy to restore mitochondrial homeostasis may be at the center of a large range of translational opportunities for improving human health.
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