Key result
Overexpression of TNNI3K in transgenic mice promoted physiological concentric cardiac hypertrophy with a 1.31-fold increase in heart weight to body weight ratio and enhanced cardiac function.
Why the study?
Does overexpression of TNNI3K promote physiological cardiac hypertrophy in transgenic mice?
Does overexpression of TNNI3K promote physiological cardiac hypertrophy in transgenic mice?
Effect estimate: 1.31 fold increase
Absolute Event Rate: 6.7% vs 5.1%
p-value: p=<0.01
TNNI3K overexpression promotes physiological concentric cardiac hypertrophy with enhanced cardiac function via cTnI phosphorylation, suggesting it as a potential therapeutic target for heart failure.
TNNI3K overexpression induces physiological hypertrophy in mice; leaves open its relevance as a human heart failure target.
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Wang et al. (2013) studied Cardiac Hypertrophy. TNNI3K overexpression vs. Non-transgenic littermates was evaluated on Heart weight to body weight ratio (HW/BW) at 3 months (1.31 fold increase, p=<0.01). Overexpression of TNNI3K in transgenic mice promoted physiological concentric cardiac hypertrophy with a 1.31-fold increase in heart weight to body weight ratio and enhanced cardiac function.
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