Why the study?
PDE5 inhibition activates PKG and ameliorates heart failure, but its impact on cardiac mitochondrial regulation has not been fully determined.
Does PDE5 inhibition with sildenafil improve cardiac function and remodeling via the PKG-PGC1α axis in a mouse model of pressure overload-induced heart failure?
Population
PGC1α +/+ and PGC1α -/- mice exposed to transverse aortic constriction, and cultured cardiomyocytes
Comparison
Sildenafil treatment vs untreated or PGC1α null controls
Design
Preclinical animal and cellular experimental study
Follow-up
7 weeks
Authors
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PGC1α may mediate PDE5i cardioprotection in murine pressure-overload HF; leaves open human relevance and clinical translation.
Does PDE5 inhibition with sildenafil improve cardiac function and remodeling via the PKG-PGC1α axis in a mouse model of pressure overload-induced heart failure?
The cardioprotective effects of PDE5 inhibition in heart failure are mediated through the PKG-PGC1α signaling axis, highlighting a key mitochondrial regulatory mechanism.
Zhu et al. (2021) studied this question.
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