Key result
Expression of a beta-adrenergic phospho-mimetic of cardiac troponin I (cTnI S23/24D) accelerated baseline myocyte relaxation and blunted further isoproterenol-induced hastening (7.2 ms vs 31.2 ms).
Population
Transgenic mice bearing near complete replacement of native cTnI with a beta-adrenergic phospho-mimetic of…
Comparison
Transgenic replacement or gene transfer of cTnI… vs Nontransgenic control mice/myocytes and gene…
Design
Preclinical
Authors
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No immediate clinical implications; leaves open cTnI phosphorylation as a lusitropic target for further study.
Absolute Event Rate: 7.2% vs 31.2%
Cardiac troponin I phosphorylation plays a key direct role in accelerating cardiac myocyte relaxation performance during beta-adrenergic stimulation.
Yasuda et al. (2007) studied Cardiac myocyte relaxation. cTnI S23/24D transgenic expression or gene transfer vs. Nontransgenic controls or wild-type cTnI was evaluated on Isoproterenol-induced change in relaxation time (delta Iso). Expression of a beta-adrenergic phospho-mimetic of cardiac troponin I (cTnI S23/24D) accelerated baseline myocyte relaxation and blunted further isoproterenol-induced hastening (7.2 ms vs 31.2 ms).
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