Key result
Smad7 knockout mice developed more severe cardiac injury in response to Angiotensin II infusion, demonstrated by a significant increase in left ventricular mass (P<0.01) and reduction of left ventricular ejection fraction (P<0.001).
Why the study?
Does Smad7 deficiency enhance cardiac remodeling and dysfunction induced by Angiotensin II infusion in a mouse model?
Population
Smad7 gene knockout (KO) and wild-type (WT) mice (CD-1 background, male, aged 8-10 weeks, 30-35 g)
Comparison
Subcutaneous infusion of Angiotensin II for 28… vs Saline infusion and wild-type mice receiving…
Design
Preclinical
Follow-up
28 days
Authors
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Supports Smad7 protection in Ang II remodeling; hypothesis-generating for therapeutic targeting, should not yet change practice.
Does Smad7 deficiency enhance cardiac remodeling and dysfunction induced by Angiotensin II infusion in a mouse model?
p-value: p=<0.01
Smad7 plays a protective role against Angiotensin II-mediated cardiac remodeling, fibrosis, and inflammation, suggesting it as a potential therapeutic target for hypertensive cardiovascular disease.
Wei et al. (2013) studied Hypertensive cardiac remodeling. Smad7 gene knockout vs. Wild-type mice was evaluated on Cardiac injury (left ventricular mass, ejection fraction, and fractional shortening) (p=<0.01). Smad7 knockout mice developed more severe cardiac injury in response to Angiotensin II infusion, demonstrated by a significant increase in left ventricular mass (P<0.01) and reduction of left ventricular ejection fraction (P<0.001).
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