National Heart Research Institute Singapore, National Heart Centre, Singapore; Cardiovascular & Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore.
National Heart Research Institute Singapore, National Heart Centre, Singapore; Cardiovascular & Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore; Institute of Biochemistry, Medical School, Justus-Liebig University, 35392 Giessen, Germany.
EBioMedicine. 2020 Jul;57:102884. doi: 10.1016/j.ebiom.2020.102884. Epub 2020 Jul 10.
Acute myocardial infarction (AMI) and the heart failure (HF) that often follows are among the leading causes of death and disability worldwide. As such, new treatments are needed to protect the myocardium against the damaging effects of the acute ischaemia and reperfusion injury (IRI) that occurs in AMI, in order to reduce myocardial infarct (MI) size, preserve cardiac function, and improve patient outcomes. In this regard, cardiac mitochondria play a dual role as arbiters of cell survival and death following AMI. Therefore, preventing mitochondrial dysfunction induced by acute myocardial IRI is an important therapeutic strategy for cardioprotection. In this article, we review the role of mitochondria as key determinants of acute myocardial IRI, and we highlight their roles as therapeutic targets for reducing MI size and preventing HF following AMI. In addition, we discuss the challenges in translating mitoprotective strategies into the clinical setting for improving outcomes in AMI patients.
急性心肌梗死（AMI）和随之发生的心力衰竭（HF）是全球范围内主要的死亡和残疾原因之一。因此，需要新的治疗方法来保护心肌免受 AMI 中发生的急性缺血再灌注损伤（IRI）的破坏性影响，以减小心肌梗死（MI）面积，保护心脏功能，并改善患者预后。在这方面，心脏线粒体在 AMI 后细胞存活和死亡的裁决中发挥着双重作用。因此，预防急性心肌 IRI 引起的线粒体功能障碍是心脏保护的重要治疗策略。本文综述了线粒体作为急性心肌 IRI 关键决定因素的作用，并强调了它们作为减少 MI 面积和预防 AMI 后 HF 的治疗靶点的作用。此外，我们还讨论了将线粒体保护策略转化为改善 AMI 患者结局的临床实践所面临的挑战。
Zotero 插件
