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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.

Targeting calcium transport in ischaemic heart disease