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[潜在靶点——线粒体动力学相关蛋白在心肌缺血再灌注损伤治疗中的研究进展]

[Research progress on potential targets-mitochondrial dynamics-related proteins in treatment of myocardial ischemia-reperfusion injury].

作者信息

Man-Li Zhou, Yu Feng, Shu-le Qian, Xiao-Xin Luo, Si-Qi X U, Wei-Xiong Jian

机构信息

College of Traditional Chinese Medicine, Hunan University of Traditional Chinese Medicine Changsha 410208, China.

College of Traditional Chinese Medicine, Hunan University of Traditional Chinese Medicine Changsha 410208, China National Key Discipline of Traditional Chinese Medicine Diagnostics, Hunan Provincial Key Laboratory,Hunan University of Chinese Medicine Changsha 410208, China.

出版信息

Zhongguo Zhong Yao Za Zhi. 2020 Sep;45(17):4183-4195. doi: 10.19540/j.cnki.cjcmm.20200623.602.

DOI:10.19540/j.cnki.cjcmm.20200623.602
PMID:33164403
Abstract

Acute myocardial infarction(AMI) is still the leading cause of death worldwide. At present, the treatment of AMI is mainly to restore the cardiac blood supply through myocardial reperfusion. With the widespread use of coronary artery bypass grafting and percutaneous coronary intervention(PCI), myocardial reperfusion injury is a major clinical problem. Mitochondrial dysfunction is an important pathological basis for myocardial ischemic injury. Therefore, mitochondria can be used as an important target against myocardial damage. In this article, we would briefly review the physiological functions of mitochondrial dynamics-related proteins as well as their pathological mechanisms and pharmacological interventions in treatment of myocardial ischemia-reperfusion injury.

摘要

急性心肌梗死(AMI)仍然是全球范围内的主要死亡原因。目前,AMI的治疗主要是通过心肌再灌注来恢复心脏供血。随着冠状动脉旁路移植术和经皮冠状动脉介入治疗(PCI)的广泛应用,心肌再灌注损伤成为一个主要的临床问题。线粒体功能障碍是心肌缺血损伤的重要病理基础。因此,线粒体可作为对抗心肌损伤的重要靶点。在本文中,我们将简要综述线粒体动力学相关蛋白的生理功能及其在治疗心肌缺血-再灌注损伤中的病理机制和药物干预措施。

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Rhein alleviates myocardial ischemic injury by inhibiting mitochondrial division, activating mitochondrial autophagy and suppressing myocardial cell apoptosis through the Drp1/Pink1/Parkin pathway.瑞香素通过 Drp1/Pink1/Parkin 通路抑制线粒体分裂、激活线粒体自噬、抑制心肌细胞凋亡,从而减轻心肌缺血性损伤。
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