Key result
Transcriptional regulation of SERCA2a expression is the primary cause of decreased SERCA2a activity in heart failure, presenting potential therapeutic implications for pathologic hypertrophy.
Decreased SERCA2a activity due to transcriptional regulation is a primary driver of ventricular dysfunction in chronic heart failure, presenting a potential therapeutic target.
May guide SERCA2a research in HF; leaves open clinical translation pending prospective trials.
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.
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Muller et al. (2005) conducted a review in Ventricular Hypertrophy and Heart Failure. Transcriptional regulation of SERCA2a expression is the primary cause of decreased SERCA2a activity in heart failure, presenting potential therapeutic implications for pathologic hypertrophy.
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