Key result
S100A1 overexpression preserved global contractile performance, prevented cardiac hypertrophy and heart failure, and resulted in superior survival after myocardial infarction compared to controls.
Why the study?
Does S100A1 protein level determine contractile performance and propensity toward heart failure after myocardial infarction in mice?
Population
S100A1-transgenic, S100A1-knockout, nontransgenic littermate control, and wild-type mice subjected to…
Comparison
S100A1 overexpression or S100A1 knockout vs Nontransgenic littermate control and wild-type…
Design
Preclinical
Follow-up
up to 4 weeks
Authors
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Hypothesis-generating for S100A1-targeted post-MI therapy in mice; leaves open translation to humans.
Does S100A1 protein level determine contractile performance and propensity toward heart failure after myocardial infarction in mice?
Downregulation of S100A1 protein critically contributes to contractile dysfunction after myocardial infarction, while its overexpression preserves function and survival in a mouse model.
Most et al. (2006) studied Myocardial infarction and heart failure. S100A1 overexpression (STG) or knockout (SKO) vs. Nontransgenic littermate control (NLC) and wild-type (WT) was evaluated on Survival, cardiac function, and remodeling. S100A1 overexpression preserved global contractile performance, prevented cardiac hypertrophy and heart failure, and resulted in superior survival after myocardial infarction compared to controls.
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