Regulation of myocardial SERCA2a expression in ventricular hypertrophy and heart failure.
Diminished contractility of the hypertrophic cardiomyocyte is a principal determinant of ventricular dysfunction in chronic heart failure. Reduction of activity of the sarcoplasmic/endoplasmic reticulum calcium ion (Ca2+)-ATPase (SERCA2a), underlies many of the effects of overload-induced hypertrophy on cardiomyocyte performance, and it may be critical in the progression of compensatory hypertrophy to heart failure. This review shall focus on the transcriptional regulation of SERCA2a expression as the primary cause of decreased SERCA2a activity in heart failure. Furthermore, the relevance for SERCA2a expression of signal transduction routes involved in pathologic hypertrophy and the possible therapeutic implications, shall be addressed.
Institute for Cardiovascular Research, Laboratory for Physiology, VU University Medical Center, Van der Boechorststraat 7, 1081 BT Amsterdam, The Netherlands.
Alice
A
Muller
Warner S
WS
Simonides