期刊
AUTOPHAGY
卷 18, 期 6, 页码 1216-1239出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2021.1975914
关键词
Cell metabolism; metabolite; mitochondria; mitophagy; mitophagy receptor
类别
资金
- National Natural Science Foundation of China [32070738]
- Fundamental Research Funds for the Central Universities [2662020DKPY009]
- State Key Laboratory of Medicinal Chemical Biology, Nankai University [2020015]
Mitochondria play crucial roles in cellular metabolism and regulated cell death, with mitophagy serving as a key mechanism for maintaining cellular homeostasis. Mitophagy is regulated by various endogenous metabolites and is essential for the bidirectional interplay between mitophagy and cellular metabolisms.
Owing to the dominant functions of mitochondria in multiple cellular metabolisms and distinct types of regulated cell death, maintaining a functional mitochondrial network is fundamental for the cellular homeostasis and body fitness in response to physiological adaptations and stressed conditions. The process of mitophagy, in which the dysfunctional or superfluous mitochondria are selectively engulfed by autophagosome and subsequently degraded in lysosome, has been well formulated as one of the major mechanisms for mitochondrial quality control. To date, the PINK1-PRKN-dependent and receptors (including proteins and lipids)-dependent pathways have been characterized to determine the mitophagy in mammalian cells. The mitophagy is highly responsive to the dynamics of endogenous metabolites, including iron-, calcium-, glycolysis-TCA-, NAD(+)-, amino acids-, fatty acids-, and cAMP-associated metabolites. Herein, we summarize the recent advances toward the molecular details of mitophagy regulation in mammalian cells. We also highlight the key regulations of mammalian mitophagy by endogenous metabolites, shed new light on the bidirectional interplay between mitophagy and cellular metabolisms, with attempting to provide a perspective insight into the nutritional intervention of metabolic disorders with mitophagy deficit.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据