Key result
Expression of mutant cTnT-Gln92 in transgenic mice exerted a dominant-negative effect, causing cardiac myocyte disarray, increased collagen, and a 50% reduction in the E/A ratio.
Why the study?
Does mutant human cardiac troponin T (cTnT-Gln92) exert a dominant-negative effect on cardiac structure and function in transgenic mice?
Does mutant human cardiac troponin T (cTnT-Gln92) exert a dominant-negative effect on cardiac structure and function in transgenic mice?
Absolute Event Rate: 2.2% vs 5.6%
p-value: p=<0.0001
Mutant cTnT-Gln92 exerts a dominant-negative effect leading to diastolic dysfunction, myocyte disarray, and increased collagen synthesis in a transgenic mouse model of hypertrophic cardiomyopathy.
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Supports dominant-negative cTnT effects in HCM mouse model; leaves open human translation and therapeutic relevance.
Oberst et al. (1998) studied Hypertrophic cardiomyopathy (n=24). Mutant human cardiac troponin T (cTnT-Gln92) transgene vs. Normal human cTnT (cTnT-Arg92) transgene and normal littermates was evaluated on E/A ratio of mitral inflow velocities (diastolic function) (p=<0.0001). Expression of mutant cTnT-Gln92 in transgenic mice exerted a dominant-negative effect, causing cardiac myocyte disarray, increased collagen, and a 50% reduction in the E/A ratio.
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