Key result
Klf9 restoration worsens pressure overload-induced systolic dysfunction, lowering LVEF to ~39% vs ~54% in controls.
Population
Mice undergoing transverse aortic constriction induced hypertrophy or sham operations
Comparison
Inducible conditional Klf9 knock-in subjected to… vs Wild-type mice subjected to TAC, and…
Design
Preclinical
Follow-up
2 weeks
Authors
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In a mouse model of pressure overload-induced hypertrophy, dysregulated Klf9 expression precipitates early cardiac dysfunction, highlighting its critical role in metabolic homeostasis.
Absolute Event Rate: 38.65% vs 53.88%
In a mouse model of pressure overload-induced hypertrophy, dysregulated Klf9 expression precipitates early cardiac dysfunction, highlighting its critical role in metabolic homeostasis.
Venkatasubramanian et al. (2025) studied Cardiac hypertrophy. Klf9 knock-in (Klf9KI) with transverse aortic constriction (TAC) vs. Wild-type with TAC (Wt-TAC) was evaluated on Ejection fraction (%EF). Restoring Klf9 levels in mice undergoing transverse aortic constriction resulted in systolic dysfunction (%EF 38.65 vs 53.88 in wild-type) without significant changes in LV mass.
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