Davis Heart and Lung Institute and The Division of Cardiovascular Medicine, Department of Internal Medicine, The Ohio State University College of Medicine, Columbus, OH 43210, USA.
Cardiovasc Res. 2009 Dec 1;84(3):345-52. doi: 10.1093/cvr/cvp264. Epub 2009 Jul 29.
Ischaemic heart disease (IHD) is the leading cause of morbidity and mortality worldwide. While timely reperfusion of acutely ischaemic myocardium is essential for myocardial salvage, it leads to a unique type of injury known as 'myocardial ischaemia/reperfusion (I/R) injury'. Growing evidence suggests that a defect in myocardial Ca(2+) transport system with cytosolic Ca(2+) overload is a major contributor to myocardial I/R injury. Progress in molecular genetics and medicine in past years has clearly demonstrated that modulation of Ca(2+) handling pathways in IHD could be cardioprotective. The potential benefits of these strategies in limiting I/R injury are vast, and the time is right for challenging in vivo systemic work both at pre-clinical and clinical levels.
缺血性心脏病（IHD）是全球发病率和死亡率的主要原因。虽然急性缺血心肌的及时再灌注对于心肌挽救至关重要，但它会导致一种称为“心肌缺血/再灌注（I / R）损伤”的独特损伤类型。越来越多的证据表明，细胞溶质 Ca（2+）超载导致心肌 Ca（2+）转运系统缺陷是心肌 I / R 损伤的主要原因。过去几年分子遗传学和医学的进展清楚地表明，调节 IHD 中的 Ca（2+）处理途径可能具有心脏保护作用。这些策略在限制 I / R 损伤方面的潜在益处是巨大的，现在正是在临床前和临床水平上挑战体内全身性工作的合适时机。
