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• W1979622294 abstract "Heart failure is characterised by depressed myocyte contractility and is considered to involve a complex malfunction of adrenergic regulation, Ca2+-handling and the contractile apparatus. Most studies on the contractile apparatus have focussed on troponin, the Ca2+-dependent regulator of myofibrillar activity. Importantly, phosphorylation of troponin I secondary to beta-adrenergic receptor activation is known to induce reduced myofilament Ca2+sensitivity. In muscle samples from explanted failing human hearts, troponin I phosphorylation levels are very low and Ca2+-sensitivity is high. In contrast, some animal models used to study the mechanisms of heart failure give the opposite result-high levels of troponin I phosphorylation and low Ca2+-sensitivity. Which is right?" @default.
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• W1979622294 date "2008-11-01" @default.
• W1979622294 modified "2023-09-29" @default.
• W1979622294 title "Troponin phosphorylation and myofilament Ca2+-sensitivity in heart failure: Increased or decreased?" @default.
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• W1979622294 doi "https://doi.org/10.1016/j.yjmcc.2008.07.004" @default.
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