Key result
Experimental LV hypertrophy and congestive heart failure in rats are associated with depressed myofilament Ca2+ sensitivity, partly due to augmented phosphorylation of cTnI.
Why the study?
Does troponin exchange alter myofilament Ca2+ sensitivity in rat models of LV hypertrophy and congestive heart failure?
Population
Rat models of pressure overload-induced left ventricular hypertrophy and myocardial infarction-elicited…
Comparison
Treatment of a subset of cells with either… vs Control myocytes, or cells without troponin…
Design
Preclinical
Authors
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Depressed myofilament Ca2+ sensitivity in rat LVH/CHF models warrants no clinical change; hypothesis-generating for cTnI phosphorylation as therapeutic target.
Does troponin exchange alter myofilament Ca2+ sensitivity in rat models of LV hypertrophy and congestive heart failure?
Depressed myofilament Ca2+ sensitivity in experimental LVH and CHF is partly due to a decreased functional role of cTn, likely involving augmented phosphorylation of cTnI.
Belin et al. (2006) studied Left ventricular hypertrophy and congestive heart failure. Recombinant cardiac troponin (cTn) or purified cTn exchange vs. Control myocytes or untreated failing myocytes was evaluated on Myofilament function characterized by force-[Ca2+] relation (Fmax, EC50, nH). Experimental LV hypertrophy and congestive heart failure in rats are associated with depressed myofilament Ca2+ sensitivity, partly due to augmented phosphorylation of cTnI.
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