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    Physiology (Bethesda). 2008 Feb;23:6-16.

    Toward biologically targeted therapy of calcium cycling defects in heart failure.

    Ikeda Y, Hoshijima M, Chien KR.

    Department of Molecular Cardiovascular Biology, Yamaguchi University School of Medicine, Ube, Japan. ysikeda@yamaguchi-u.ac.jp

    A growing body of evidence indicates that heart failure progression is tightly associated with dysregulation of phosphorylation of Ca2+ regulators localized in the sub-cellular microdomain of the sarcoplasmic reticulum. Chemical or genetic correction of abnormalities in cardiac phosphorylation cascades is emerging as a potential target in the treatment of heart failure. Here, we review how specific kinases and phosphatases finely tune Ca2+ cycling and regulate excitation-contraction (E-C) coupling in cardiomyocytes.

    PMID: 18268360 [PubMed - indexed for MEDLINE]

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