Key result
Epac1 deletion protected mice from cardiac dysfunction, apoptosis, and fibrosis induced by various stresses including pressure overload, chronic isoproterenol, and aging.
Why the study?
Does Epac1 deletion protect the heart from stress-induced cardiomyopathy and regulate cardiac contractility in mice?
Population
Mice (Epac1 knockout, Epac2 knockout, and wild-type) and isolated cardiomyocytes
Comparison
Epac1 deletion and direct EPAC activation vs Wild-type (WT) mice and Epac2 deletion
Design
Preclinical
Authors
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Epac1 deletion protects stressed mouse hearts; leaves open its viability as a human therapeutic target.
Does Epac1 deletion protect the heart from stress-induced cardiomyopathy and regulate cardiac contractility in mice?
Absolute Event Rate: 60% vs 54%
p-value: p=<0.01
Epac1 is a crucial regulator of PKA-independent phospholamban phosphorylation, and its deletion protects against stress-induced cardiomyopathy, highlighting it as a potential therapeutic target.
Okumura et al. (2014) studied Cardiac stress response and heart failure. Epac1 deletion vs. Wild-type mice was evaluated on Left ventricular ejection fraction (LVEF) at 3 weeks after aortic banding (p=<0.01). Epac1 deletion protected mice from cardiac dysfunction, apoptosis, and fibrosis induced by various stresses including pressure overload, chronic isoproterenol, and aging.
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