Open AccessMitophagy Disequilibrium, a Prominent Pathological Mechanism in Metabolic Heart Diseases
Author(s) -
Yunhao Li,
Ningning Zheng,
Xiwei Ding
Publication year - 2021
Publication title -
diabetes, metabolic syndrome and obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.853
H-Index - 43
ISSN - 1178-7007
DOI - 10.2147/dmso.s336882
Subject(s) - mitophagy , parkin , mitochondrion , biology , autophagy , reactive oxygen species , homeostasis , population , microbiology and biotechnology , hypoxia (environmental) , heart failure , medicine , apoptosis , oxygen , genetics , chemistry , disease , environmental health , organic chemistry , parkinson's disease
With overall food intake among the general population as high as ever, metabolic syndrome (MetS) has become a global epidemic and is responsible for many serious life-threatening diseases, especially heart failure. In multiple metabolic disorders, maintaining a dynamic balance of mitochondrial number and function is necessary to prevent the overproduction of reactive oxygen species (ROS), which has been proved to be one of the important mechanisms of cardiomyocyte injury due to the mismatching of oxygen consumption and mitochondrial population and finally to heart failure. Mitophagy is a process that eliminates damaged or redundant mitochondria. It is mediated by a series of signaling molecules, including PINK, parkin, BINP3, FUNDC1, CTSD, Drp1, Rab9 and mTOR. Meanwhile, increasing evidence also showed that the interaction between ferroptosis and mitophagy interfered with mitochondrial homeostasis. This review will focus on these essential molecules and pathways of mitophagy and cell homeostasis affected by hypoxia and other stimuli in metabolic heart diseases.