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- W2330389384 abstract "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." @default.
- W2330389384 created "2016-06-24" @default.
- W2330389384 creator A5015602245 @default.
- W2330389384 creator A5046419671 @default.
- W2330389384 creator A5052656125 @default.
- W2330389384 creator A5058968063 @default.
- W2330389384 creator A5067342400 @default.
- W2330389384 creator A5068607724 @default.
- W2330389384 creator A5070801202 @default.
- W2330389384 date "2016-01-01" @default.
- W2330389384 modified "2023-10-17" @default.
- W2330389384 title "The Role of Mitochondrial Functional Proteins in ROS Production in Ischemic Heart Diseases" @default.
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