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Regulation of Cardiac Muscle Contraction

S100A1: a novel inotropic regulator of cardiac performance. Transition from molecular physiology to pathophysiological relevance

¹Center for Translational Medicine, Laboratory for Cardiac Stem Cell and Gene Therapy, Department of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania; and ²Department of Internal Medicine III, University of Heidelberg, Heidelberg, Germany

Here we review the considerable body of evidence that has accumulated to support the notion of S100A1, a cardiac-specific Ca²⁺-sensor protein of the EF-hand type, as a physiological regulator of excitation-contraction coupling and inotropic reserve mechanisms in the mammalian heart. In particular, molecular mechanisms will be discussed conveying the Ca²⁺-dependent inotropic actions of S100A1 protein in cardiomyocytes occurring independently of -adrenergic signaling. Moreover, we will shed light on the molecular structure-function relationship of S100A1 with its cardiac target proteins at the sarcoplasmic reticulum, the sarcomere, and the mitochondria. Furthermore, pathophysiological consequences of disturbed S100A1 protein expression on altered Ca²⁺ handling and intertwined systems in failing myocardium will be highlighted. Subsequently, therapeutic options by means of genetic manipulation of cardiac S100A1 expression will be discussed, aiming to complete our current understanding of the role of S100A1 in diseased myocardium.

excitation-contraction coupling; cardiomyocyte; heart failure; gene therapy

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