Altered sarcoplasmic reticulum calcium cycling—targets for heart failure therapy View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2012-12

AUTHORS

Changwon Kho, Ahyoung Lee, Roger J. Hajjar

ABSTRACT

Cardiac myocyte function is dependent on the synchronized movements of Ca(2+) into and out of the cell, as well as between the cytosol and sarcoplasmic reticulum. These movements determine cardiac rhythm and regulate excitation-contraction coupling. Ca(2+) cycling is mediated by a number of critical Ca(2+)-handling proteins and transporters, such as L-type Ca(2+) channels (LTCCs) and sodium/calcium exchangers in the sarcolemma, and sarcoplasmic/endoplasmic reticulum calcium ATPase 2a (SERCA2a), ryanodine receptors, and cardiac phospholamban in the sarcoplasmic reticulum. The entry of Ca(2+) into the cytosol through LTCCs activates the release of Ca(2+) from the sarcoplasmic reticulum through ryanodine receptor channels and initiates myocyte contraction, whereas SERCA2a and cardiac phospholamban have a key role in sarcoplasmic reticulum Ca(2+) sequesteration and myocyte relaxation. Excitation-contraction coupling is regulated by phosphorylation of Ca(2+)-handling proteins. Abnormalities in sarcoplasmic reticulum Ca(2+) cycling are hallmarks of heart failure and contribute to the pathophysiology and progression of this disease. Correcting impaired intracellular Ca(2+) cycling is a promising new approach for the treatment of heart failure. Novel therapeutic strategies that enhance myocyte Ca(2+) homeostasis could prevent and reverse adverse cardiac remodeling and improve clinical outcomes in patients with heart failure. More... »

PAGES

717

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nrcardio.2012.145

    DOI

    http://dx.doi.org/10.1038/nrcardio.2012.145

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1051992020

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/23090087


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