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REVIEW

Toward Biologically Targeted Therapy of Calcium Cycling Defects in Heart Failure

Yasuhiro Ikeda¹, Masahiko Hoshijima² and Kenneth R. Chien³

¹ Department of Molecular Cardiovascular Biology, Yamaguchi University School of Medicine, Ube, Japan;
² Department of Medicine, Center for Research in Biological Systems, University of California San Diego, San Diego, California; and
³ MGH Cardiovascular Research Center, Harvard Medical School, Boston, Massachusetts krchien{at}partners.org ysikeda{at}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.