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Oxidative Medicine and Cellular Longevity
Volume 2016, Article ID 5470457, 8 pages
Review Article

The Role of Mitochondrial Functional Proteins in ROS Production in Ischemic Heart Diseases

1Department of Cardiology, Chengdu Military General Hospital, Chengdu 610083, China
2Department of Cardiology, Third Military Medical University, Chongqing 400042, China
3Department of Ultrasonography, Chengdu Military General Hospital, Chengdu 610083, China

Received 23 December 2015; Revised 27 January 2016; Accepted 28 January 2016

Academic Editor: Sergio Di Meo

Copyright © 2016 Haifeng Pei et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.