Monteiro Pedro, Oliveira Paulo J, Conçalves Lino, Providência Luís A
Unidade de Investigação Básica em Cardiologia-Serviço de Cardiologia, Hospitais da Universidade de Coimbra, Coimbra.
Rev Port Cardiol. 2003 Mar;22(3):407-29.
In recent years, basic research has enabled a better understanding of the molecular and cellular basis of myocardial ischemia. In this context, cardiac mitochondria have been shown to perform an important role, being essential to energy production and ionic homeostasis, and thus controlling cardioprotection and cell death. Knowledge of these facts has led to the development of new therapeutic strategies for myocardial ischemia, aiming to modify its biochemical pathways and to preserve mitochondrial function. It has also led to a better understanding of the cellular and subcellular effects of classical anti-ischemic drugs, revealing that most of them also have a direct impact on cardiac mitochondrial function. This article summarizes what is currently known regarding the pharmacological modulation of mitochondrial function during ischemia and reperfusion and how it can induce cardioprotection in coronary artery disease patients.
近年来,基础研究使人们对心肌缺血的分子和细胞基础有了更深入的了解。在此背景下,心脏线粒体已被证明发挥着重要作用,对能量产生和离子稳态至关重要,从而控制心脏保护和细胞死亡。对这些事实的了解促使了针对心肌缺血的新治疗策略的发展,旨在改变其生化途径并维持线粒体功能。这也使人们对经典抗缺血药物的细胞和亚细胞效应有了更好的理解,表明它们中的大多数也对心脏线粒体功能有直接影响。本文总结了目前关于缺血和再灌注期间线粒体功能的药理学调节以及它如何在冠状动脉疾病患者中诱导心脏保护的已知情况。