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Am J Physiol Regul Integr Comp Physiol 293: R568-R577, 2007. First published April 25, 2007; doi:10.1152/ajpregu.00075.2007
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INVITED REVIEW

CALL FOR PAPERS
Regulation of Cardiac Muscle Contraction

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

Patrick Most,1 Andrew Remppis,2 Sven T. Pleger,2 Hugo A. Katus,2 and Walter J. Koch1

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 beta-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


Address for reprint requests and other correspondence: P. Most, Center for Translational Medicine, Dept. of Medicine, Thomas Jefferson Univ., Philadelphia, PA 19107 (e-mail: patrick.most{at}jefferson.edu)




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