Regulation of myocardial SERCA2a expression in ventricular hypertrophy and heart failure

Authors: Muller, Alice; Simonides, Warner S

Source: Future Cardiology, Volume 1, Number 4, July 2005 , pp. 543-553(11)

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Abstract:

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.

Keywords: calcium homeostasis; gene-expression regulation; heart failure; sarcoplasmic/endoplasmic reticulum Ca2+-ATPase; transcription factor; ventricular hypertrophy

Document Type: Research article

DOI: http://dx.doi.org/10.2217/14796678.1.4.543

Publication date: 2005-07-01

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Future Cardiology reflects the new era of cardiology and highlights new molecular approaches in advancing cardiovascular therapy. The journal publishes clinical research, commentary and therapeutic overviews highlighting optimal therapy and future options and strategies.
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