Abstract
The amplitude and velocity of intracellular Ca(2 +) cycling determines contractility in normal and failing hearts. Cardiac sarcoplasmic reticulum (SR) is a specialized membranous organelle which determines the property of such intracellular calcium transport in cardiomyocytes. In the SR membrane, sarco-endoplasmic reticulum ATPase (SERCA2a) sequestrates Ca(2 +) from the cytosol to the SR, thereby regulating cardiac diastolic performance. In the failing hearts, depressed SERCA2a function has been shown to be associated with impaired contractility and aberrant increase in cytosolic Ca(2 +) concentration. Therefore, molecular targeting of SERCA2a complexes becomes an emerging therapeutic target. In this review, mechanisms modifying SERCA2a function and associated topics is reviewed.
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