Send to

Choose Destination
See comment in PubMed Commons below
Am J Physiol Regul Integr Comp Physiol. 2007 Aug;293(2):R568-77. Epub 2007 Apr 25.

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

Author information

  • 1Center for Translational Medicine, Laboratory for Cardiac Stem Cell and Gene Therapy, Department of Medicine, Thomas Jefferson University, Philadelphia, PA 19107, USA.


Here we review the considerable body of evidence that has accumulated to support the notion of S100A1, a cardiac-specific Ca(2+)-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 Ca(2+)-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 Ca(2+) 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.

[PubMed - indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire
    Loading ...
    Support Center