Cardiovascular & Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore, Singapore.
National Heart Research Institute Singapore, National Heart Centre, Singapore, Singapore.
J Cell Mol Med. 2020 Jul;24(13):7102-7114. doi: 10.1111/jcmm.15341. Epub 2020 Jun 3.
Acute myocardial infarction (AMI) and the heart failure (HF) that often result remain the leading causes of death and disability worldwide. As such, new therapeutic targets need to be discovered to protect the myocardium against acute ischaemia/reperfusion (I/R) injury in order to reduce myocardial infarct (MI) size, preserve left ventricular function and prevent the onset of HF. Mitochondrial dysfunction during acute I/R injury is a critical determinant of cell death following AMI, and therefore, ion channels in the inner mitochondrial membrane, which are known to influence cell death and survival, provide potential therapeutic targets for cardioprotection. In this article, we review the role of mitochondrial ion channels, which are known to modulate susceptibility to acute myocardial I/R injury, and we explore their potential roles as therapeutic targets for reducing MI size and preventing HF following AMI.
急性心肌梗死(AMI)和由此导致的心力衰竭(HF)仍然是全球范围内导致死亡和残疾的主要原因。因此,需要发现新的治疗靶点,以保护心肌免受急性缺血/再灌注(I/R)损伤,从而减少心肌梗死(MI)面积、保护左心室功能并预防 HF 的发生。急性 I/R 损伤期间的线粒体功能障碍是 AMI 后细胞死亡的关键决定因素,因此,已知影响细胞死亡和存活的线粒体内膜离子通道为心脏保护提供了潜在的治疗靶点。在本文中,我们综述了已知可调节急性心肌 I/R 损伤易感性的线粒体离子通道的作用,并探讨了它们作为减少 AMI 后 MI 面积和预防 HF 的治疗靶点的潜在作用。