Key result
Sfrp1 overexpression significantly improved cardiac function in aged mice 7 days post-myocardial infarction, increasing fractional shortening to 33.26% compared to 14.45% in controls.
Why the study?
Aged patients with acute myocardial ischemia experience increased mortality and worse prognosis, necessitating more effective treatments targeting Wnt/β-catenin pathway deregulation.
Does Sfrp1 overexpression reduce myocardial injury and improve cardiac function in aged mice with acute myocardial ischemia?
Population
Aged mice with an established AMI model
Comparison
AAV-Sfrp1 transduction vs control
Design
Animal experimental study
Authors
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Hypothesis-generating for Sfrp1 gene therapy in aged AMI; leaves open human translation and clinical utility.
Does Sfrp1 overexpression reduce myocardial injury and improve cardiac function in aged mice with acute myocardial ischemia?
Absolute Event Rate: 33.26% vs 14.45%
p-value: p=<0.01
Sfrp1 overexpression protects against acute myocardial ischemia injury in aged mice by inhibiting the Wnt/β-catenin signaling pathway, suggesting a potential gene therapy target.
Tao et al. (2021) studied Acute myocardial ischemia (n=128). AAV-Sfrp1 vs. dsAVV9-GFP was evaluated on Left ventricular short-axis shortening rate (FS) at 7 days (p=<0.01). Sfrp1 overexpression significantly improved cardiac function in aged mice 7 days post-myocardial infarction, increasing fractional shortening to 33.26% compared to 14.45% in controls.
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