Key result
Transgenic mice expressing low levels of a truncated cardiac troponin T molecule developed cardiomyopathy characterized by 18-27% smaller hearts, decreased myocyte density, and significant diastolic dysfunction.
Why the study?
Does expression of a truncated cTnT allele induce features of familial hypertrophic cardiomyopathy in transgenic mice?
Population
Transgenic mice expressing a truncated mouse cTnT allele analogous to one found in familial hypertrophic…
Comparison
Expression of truncated cardiac troponin T (cTnT) vs Wild type mice
Design
Preclinical
Authors
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This mouse model aids mechanistic cTnT research; leaves open human HCM relevance and precludes clinical translation.
Does expression of a truncated cTnT allele induce features of familial hypertrophic cardiomyopathy in transgenic mice?
A transgenic mouse model expressing truncated cTnT recapitulates key features of familial hypertrophic cardiomyopathy, including myocellular disarray and cardiac dysfunction, suggesting multiple cellular mechanisms drive the disease.
Tardiff et al. (1998) studied Familial hypertrophic cardiomyopathy. Truncated cardiac troponin T (cTnT) transgene vs. Wild-type (WT) or non-transgenic mice was evaluated. Transgenic mice expressing low levels of a truncated cardiac troponin T molecule developed cardiomyopathy characterized by 18-27% smaller hearts, decreased myocyte density, and significant diastolic dysfunction.
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