Altered sarcoplasmic reticulum calcium cycling--targets for heart failure therapy.

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 phosphol

SUBMITTER: Kho C 

PROVIDER: S-EPMC3651893 | biostudies-literature | 2012 Dec

REPOSITORIES: biostudies-literature