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线粒体蛋白在缺血性心脏病活性氧生成中的作用
周宏,罗涵,马李杰
0
(西部战区总医院呼吸内科)
摘要:
【摘要】 缺血性心脏病(IHD)每年可造成超过700万人死亡,已成为导致死亡的重要原因。缺血性心脏病时冠状动脉堵塞会造成心肌细胞的不可逆损伤甚至死亡。作为调控心肌细胞能量及凋亡的重要细胞器,线粒体在缺血性心脏病中发挥着关键调节作用。缺血损伤可降低心肌ATP产量,导致能量供应不足及活性氧(ROS)过量产生。迄今为止,许多研究表明线粒体蛋白质如电子传递链(ETC)复合物、解偶联蛋白(UCP)、线粒体动态蛋白、线粒体外膜转位酶(Tom)复合物、线粒体通透性转换孔(MPTP)等可直接或间接地影响线粒体ROS的产生,从而决定线粒体功能障碍和心肌损害的程度。本文将对目前缺血性心脏病中线粒体功能蛋白与活性氧生成两者之间关系的相关研究结果作一综述。
关键词:  缺血性心脏病  线粒体蛋白  活性氧
DOI:
基金项目:四川省科技厅科技计划项目(2014JY0149)
The role of mitochondrial proteins in ROS production in ischemic heart diseases
ZHOU Hong,LUO Han,MA Lijie
(Department of Respiratory Medicine, West theater General Hospital)
Abstract:
【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. Ischemia insult can reducemyocardial 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 outermembrane (Tom) complex, andmitochondrial 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.
Key words:  Ischemic heart diseases  Mitochondrial proteins  Reactive oxygen species

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