| Abstract: | ![]()
Various proteins such as Ca2+channels, Ca2+-pump ATPase, Na+–Ca2+exchanger, and Na+-K+ATPase in the sarcolemmal (SL) membrane are considered to be intimately involved in Ca2+-influx and Ca2+-efflux processes in the cardiomyocyte. On the other hand, Ca2+-pump ATPase, Ca2+-release channels, Ca2+-regulatory protein (phospholamban), and Ca2+-binding protein (calsequestrin) in the sarcoplasmic reticulum (SR) are known to participate in raising and lowering the intracellular concentration of Ca2+for the occurrence of cardiac contraction and relaxation processes. Therefore, a defect in any of the SL and SR proteins can be seen to result in Ca2+-handling abnormalities in cardiomyocytes and subsequently in cardiac dysfunction during the development of heart failure. In this review, evidence is presented to show that changes in the expression of genes specific for cardiac membrane proteins may lead to remodeling of both SR and SL membranes during the development of heart failure. Although a great deal of work on changes in gene expression for the SR membrane proteins has been carried out in the failing heart, relatively little information regarding changes in gene expression for SL proteins has appeared in the literature. Prevention of remodeling of cardiac membranes by modification of changes in the gene expression is suggested to serve as an important target for the treatment of heart failure. |
