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Abstract
Heart failure is a growing global health burden, which often stems from impaired contractile function at the myofilament and cellular levels. In healthy hearts, myofilaments become more sensitive to Ca2+ as myocytes are stretched. This effect is called length-dependent activation of contraction and reflects the cellular basis of the Frank-Starling mechanism. The molecular mechanisms underlying length-dependent activation remain unclear, but may involve the thick-filament regulation pathway associated with the myosin OFF- (i.e.
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