Diabetes, Metabolic Syndrome and Obesity (Nov 2021)
Mitophagy Disequilibrium, a Prominent Pathological Mechanism in Metabolic Heart Diseases
Abstract
Yunhao Li,1,* Ningning Zheng,2,* Xudong Ding3 1The First Clinical College, China Medical University, Shenyang, Liaoning, People’s Republic of China; 2Department of Pathophysiology, College of Basic Medical Science, China Medical University, Shenyang, Liaoning, People’s Republic of China; 3Department of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, Liaoning, People’s Republic of China*These authors contributed equally to this workCorrespondence: Xudong DingDepartment of Anesthesiology, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Shenyang, 110004, People’s Republic of ChinaTel +8618940257698Email [email protected]: 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.Keywords: mitophagy, metabolic heart diseases, metabolic syndrome, PTEN induced putative kinase, PINK, parkin, Bcl-2/E1B19kDa-interacting protein, BNIP3, FUN14 domain-containing protein 1, FUNDC1, ferroptosis
