Cardiac troponin I (cTnI) is a key regulatory protein in cardiac muscle contraction and
relaxation, linking Ca2+–troponin C binding with activation of crossbridge reactions with the …

During the past 5 years there has been an increasing body of literature describing the roles
cardiac myosin binding protein C (cMyBP-C) phosphorylation play in regulating cardiac …

▪ Abstract Although well known as the location of the mechanism by which the cardiac
sarcomere is activated by Ca2+ to generate force and shortening, the thin filament is now …

Troponin is essential for the regulation of cardiac contraction. Troponin is a sarcomeric
molecular switch, directly regulating the contractile event in concert with intracellular calcium …

Acute β-adrenergic stimulation enhances cardiac contractility, accelerates muscle
relaxation, and amplifies the inotropic and lusitropic response to increased stimulation …

It is becoming clear that upregulated protein kinase C (PKC) signaling plays a role in
reduced ventricular myofilament contractility observed in congestive heart failure. However …

There is evidence that multi-site phosphorylation of cardiac troponin I (cTnI) by protein
kinase C is important in both long-and short-term regulation of cardiac function. To …

An altered cardiac myofilament response to activating Ca 2+ is a hallmark of human heart
failure. Phosphorylation of cardiac troponin I (cTnI) is critical in modulating contractility and …

Heart failure with reduced ejection fraction involves activation of the sympathetic nervous
system and chronic hyperactivation of the sympatho-adrenergic receptors (ARs) β-ARs and …

Myocardial contraction is initiated upon the release of calcium into the cytosol from the
sarcoplasmic reticulum following membrane depolarization. The fundamental physiological …