Key result
SMAD2 inhibition with SM16 preserved cardiac function in mice subjected to aortic banding, increasing fractional shortening by 38% compared to controls (P≤0.05).
Why the study?
Does SM16 preserve cardiac function and attenuate remodeling in mice subjected to pressure overload via aortic banding?
Does SM16 preserve cardiac function and attenuate remodeling in mice subjected to pressure overload via aortic banding?
p-value: p=≤0.05
Pharmacological inhibition of SMAD2 signaling with SM16 attenuates cardiomyocyte hypertrophy and preserves cardiac function in a mouse model of pressure overload.
No takes yet. Share an insight, caveat, or question.
SM16 should not yet inform clinical practice; leaves open whether SMAD2 inhibition attenuates human pressure-overload remodeling.
Bjørnstad et al. (2011) studied Left ventricular pressure overload. SM16 (SMAD2 inhibitor) vs. Aortic banding without SM16 was evaluated on Cardiac function (fractional shortening) (p=≤0.05). SMAD2 inhibition with SM16 preserved cardiac function in mice subjected to aortic banding, increasing fractional shortening by 38% compared to controls (P≤0.05).
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