The Role of Mitochondrial Functional Proteins in ROS Production in Ischemic Heart Diseases.
Ischemic heart diseases (IHD) have become the leading cause of death around the world, killing more than 7 million people annually. In IHD, the blockage of coronary vessels will cause irreversible cell injury and even death. As the "powerhouse" and "apoptosis center" in cardiomyocytes, mitochondria play critical roles in IHD. Ischemia insult can reduce myocardial ATP content, resulting in energy stress and overproduction of reactive oxygen species (ROS). Thus, mitochondrial abnormality has been identified as a hallmark of multiple cardiovascular disorders. To date, many studies have suggested that these mitochondrial proteins, such as electron transport chain (ETC) complexes, uncoupling proteins (UCPs), mitochondrial dynamic proteins, translocases of outer membrane (Tom) complex, and mitochondrial permeability transition pore (MPTP), can directly or indirectly influence mitochondria-originated ROS production, consequently determining the degree of mitochondrial dysfunction and myocardial impairment. Here, the focus of this review is to summarize the present understanding of the relationship between some mitochondrial functional proteins and ROS production in IHD.
Department of Cardiology, Chengdu Military General Hospital, Chengdu 610083, China; Department of Cardiology, Third Military Medical University, Chongqing 400042, China.
Haifeng
H
Pei
Department of Cardiology, Chengdu Military General Hospital, Chengdu 610083, China.
Yi
Y
Yang
Department of Ultrasonography, Chengdu Military General Hospital, Chengdu 610083, China.
Heng
H
Zhao
Department of Cardiology, Chengdu Military General Hospital, Chengdu 610083, China.
Xiuchuan
X
Li
Department of Cardiology, Chengdu Military General Hospital, Chengdu 610083, China.
Dachun
D
Yang
Department of Cardiology, Chengdu Military General Hospital, Chengdu 610083, China.
De
D
Li
Department of Cardiology, Chengdu Military General Hospital, Chengdu 610083, China; Department of Cardiology, Third Military Medical University, Chongqing 400042, China.
Yongjian
Y
Yang
D000818:Animals; D004579:Electron Transport; D006801:Humans; D008928:Mitochondria / Q000378:metabolism; D024101:Mitochondrial Proteins / Q000378:metabolism*; D008954:Models, Biological; D017202:Myocardial Ischemia / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*
D024101:Mitochondrial Proteins; D017382:Reactive Oxygen Species