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Weighing in on Heart Failure: The Role of SERCA2a SUMOylation
RJ Schwartz... - Circulation Research, 2012 - Am Heart Assoc1. From the Department of Biology and Biochemistry University of Houston (RJS), Stem Cell Laboratory Texas Heart Institute (RJS), and Department of Cardiology (ETHY), The University of Texas MD Anderson Cancer Center, Houston, Texas.
Heart failure is a complex clinical syndrome resulting from structural changes in the myocardium that affects the ability of the ventricle to fill with or eject blood.1 It affects at least 5 million patients in the United States and consumes over 6% of our health care budget.1 Nearly half a million new patients are diagnosed to have heart failure each year and the incidence of new cases are increasing each year due to aging of the population and conversion of acute cardiac problems into chronic disorders. Coronary artery disease is the cause of heart failure in about two thirds of patients with left ventricular dysfunction. Without the ability for complete renewal, loss of functional cardiac myocytes due to MI or other causes will eventually lead to deterioration of myocardial function, resulting in heart failure.
Heart failure is characterized by the impaired efflux of cytosolic Ca2+ from the cell due to a sustained defect in SR Ca2+ reloading and release.2 A reduced expression and/or activity of the calcium-transporting AT Pase ATP2A2, also known as SERCA2a, is responsible for Ca reuptake during excitation–contraction coupling.3 Over the last decade or more, defective Ca2+ uptake resulting from decreased expression and reduced activity of SERCA2a is recognized as a ...
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Weighing in on Heart Failure: The Role of SERCA2a SUMOylation |
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