Key result
Estrogen receptor-α non-nuclear signaling conferred protection against pressure overload-induced cardiac remodeling and was indispensable for the therapeutic efficacy of PDE5 inhibition.
Why the study?
Does estrogen receptor-α non-nuclear signaling mediate cardioprotection and the efficacy of cGMP-PDE5 inhibition in mice with pressure overload-induced cardiac remodeling?
Population
Genetically engineered mice lacking estrogen receptor-α non-nuclear signaling
Comparison
cGMP-PDE5 inhibition vs soluble guanylate cyclase stimulation
Design
Animal experimental study
Authors
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ERα non-nuclear signaling mediates PDE5 inhibitor efficacy against murine pressure overload remodeling; leaves open translation to human HF therapy.
Does estrogen receptor-α non-nuclear signaling mediate cardioprotection and the efficacy of cGMP-PDE5 inhibition in mice with pressure overload-induced cardiac remodeling?
Estrogen receptor-α non-nuclear signaling is essential for the cardioprotective effects of PDE5 inhibitors, suggesting soluble guanylate cyclase stimulators may be a better therapeutic option for heart failure in post-menopausal women.
Fukuma et al. (2020) studied Cardiac remodeling induced by pressure overload. Estrogen receptor-α non-nuclear signaling was evaluated on Cardiac remodeling induced by pressure overload. Estrogen receptor-α non-nuclear signaling conferred protection against pressure overload-induced cardiac remodeling and was indispensable for the therapeutic efficacy of PDE5 inhibition.
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