Institute of Pharmacy and Pharmacology, Hunan province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, China.
Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, Hunan International Scientific and Technological Cooperation Base of Arteriosclerotic Disease, Hengyang Medical School, University of South China, Hengyang, China.
J Drug Target. 2022 Sep;30(8):833-844. doi: 10.1080/1061186X.2022.2085728. Epub 2022 Jun 28.
Myocardial ischaemia-reperfusion injury (MI/RI) refers to the further damage done to ischaemic cardiomyocytes when restoring blood flow. A large body of evidence shows that MI/RI is closely associated with excessive production of mitochondrial reactive oxygen species, mitochondrial calcium overload, disordered mitochondrial energy metabolism, mitophagy, mitochondrial fission, and mitochondrial fusion. According to the way it affects mitochondria, it can be divided into mitochondrial quality abnormalities and mitochondrial quantity abnormalities. Abnormal mitochondrial quality refers to the dysfunction caused by the severe destruction of mitochondria, which then affects the balance of mitochondrial density and number, causing an abnormal mitochondrial quantity. In the past, most of the reports were limited to the study of the mechanism of myocardial ischaemia-reperfusion injury, some of which involved mitochondria, but no specific countermeasures were proposed. In this review, we outline the mechanisms for treating myocardial ischaemia-reperfusion injury from the direction of mitochondria and focus on targeted interventions and drugs to restore mitochondrial health during abnormal mitochondrial quality control and abnormal mitochondrial quantity control. This is an update in the field of myocardial ischaemia-reperfusion injury.
心肌缺血再灌注损伤(MI/RI)是指恢复血流时对缺血性心肌细胞造成的进一步损伤。大量证据表明,MI/RI 与线粒体活性氧的过度产生、线粒体钙超载、线粒体能量代谢紊乱、自噬、线粒体分裂和线粒体融合密切相关。根据其对线粒体的影响方式,可分为线粒体质量异常和线粒体数量异常。异常的线粒体质量是指线粒体严重破坏引起的功能障碍,进而影响线粒体密度和数量的平衡,导致线粒体数量异常。过去,大多数报道仅限于对心肌缺血再灌注损伤机制的研究,其中一些涉及线粒体,但没有提出具体的对策。在这篇综述中,我们从线粒体的方向概述了治疗心肌缺血再灌注损伤的机制,并重点关注靶向干预和药物,以在异常线粒体质量控制和异常线粒体数量控制期间恢复线粒体健康。这是心肌缺血再灌注损伤领域的最新进展。