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Am J Physiol Regul Integr Comp Physiol (April 25, 2007). doi:10.1152/ajpregu.00075.2007
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Submitted on February 1, 2007
Accepted on April 20, 2007

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

Patrick Most1*, Andrew Remppis2, Sven T Pleger2, Hugo A Katus2, and Walter J. Koch3

1 Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania, United States
2 Medicine III, University of Heidelberg, Heidelberg, Germany
3 Translational Medicine, Jefferson Medical College, Philadelphia, Pennsylvania, United States

* To whom correspondence should be addressed. E-mail: patrick.most{at}jefferson.edu.

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 (ec) 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. Moreover, we will shed light on structure-function relationship of S100A1 with its cardiac target proteins at the sarcoplasmic reticulum, the sarcomere and mitochondria. Furthermore, pathophysiological consequences of disturbed S100A1 protein expression on altered Ca2+ handling in failing myocardium will be highlighted. Subsequently, novel therapeutic options by the means of genetic manipulation of cardiac S100A1 expression will be discussed aiming to complete our current understanding of S100A1 role in diseased myocardium.




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