Abstract
A common characteristic of the failing cardiomyocyte is abnormal calcium homeostasis, manifested by prolonged calcium transients and changes in systolic and diastolic calcium levels [1] and linked to depressed sarcoplasmic reticulum (SR) calcium cycling [2,3]. The SR acts as a calcium source during contraction and a calcium sink during relaxation. Relaxation is mediated by the transport of calcium from the cytosol into the lumen of the SR by a cardiac-specific sarco(endo)plasmic reticulum Ca 2+ -ATPase, SERCA2a, whose activity is regulated by a small phosphoprotein called phospholamban (PLN). In this review, the role of PLN in the pathogenesis of heart failure is discussed. Specifically, the functional effects of several naturally occurring PLN mutations in humans are examined, and the potential of PLN as a therapeutic target in human heart failure is assessed.
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