title: Targeting calcium transport in ischaemic heart disease.
abstract: 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.
authors.affiliation: 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.
authors.forename: M A Hassan
authors.initials: MA
authors.lastname: Talukder
authors.forename: Jay L
authors.initials: JL
authors.lastname: Zweier
authors.forename: Muthu
authors.initials: M
authors.lastname: Periasamy
mesh_terms: D001692:Biological Transport / Q000502:physiology; D002118:Calcium / Q000378:metabolism*; D020746:Calcium Channels, L-Type / Q000378:metabolism; D006801:Humans; D017202:Myocardial Ischemia / Q000378:metabolism* / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases / Q000378:metabolism; D019831:Sodium-Calcium Exchanger / Q000378:metabolism
chemical_list: D020746:Calcium Channels, L-Type; D019831:Sodium-Calcium Exchanger; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D002118:Calcium