Key result
Transgenic expression of slow skeletal troponin I in mouse cardiomyocytes resulted in impaired diastolic function and a lack of contractile responsiveness to beta-adrenergic receptor stimulation.
Population
Transgenic mice expressing slow skeletal troponin I (ssTnI) specifically in cardiomyocytes
Comparison
Transgenic replacement of cardiac troponin I… vs Wild-type control mice and non-transgenic…
Design
Preclinical
Authors
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No immediate clinical implications; leaves open troponin I as a target in diastolic dysfunction models.
Cardiac troponin I is required for normal cardiomyocyte relaxation, diastolic function, and beta-adrenergic responsiveness.
Fentzke et al. (1999) studied Impaired cardiomyocyte relaxation and diastolic function. Transgenic expression of slow skeletal troponin I (ssTnI) vs. Wild-type controls was evaluated on Cardiomyocyte relaxation and diastolic function. Transgenic expression of slow skeletal troponin I in mouse cardiomyocytes resulted in impaired diastolic function and a lack of contractile responsiveness to beta-adrenergic receptor stimulation.
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