The Role of Mitochondrial Functional Proteins in ROS Production in Ischemic Heart Diseases.
The Role of Mitochondrial Functional Proteins in ROS Production in Ischemic Heart Diseases.
复制标题
线粒体功能蛋白在缺血性心脏病中 ROS 产生的作用
DOI：
10.1155/2016/5470457
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发表时间：
2016
影响因子：
--
通讯作者：
Yang Y
中科院分区：
文献类型：
--
作者：
Pei H;Yang Y;Zhao H;Li X;Yang D;Li D;Yang Y
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.
