title: Cardiac myofilaments: mechanics and regulation.
abstract: The mechanical properties of the cardiac myofilament are an important determinant of pump function of the heart. This report is focused on the regulation of myofilament function in cardiac muscle. Calcium ions form the trigger that induces activation of the thin filament which, in turn, allows for cross-bridge formation, ATP hydrolysis, and force development. The structure and protein-protein interactions of the cardiac sarcomere that are responsible for these processes will be reviewed. The molecular mechanism that underlies myofilament activation is incompletely understood. Recent experimental approaches have been employed to unravel the mechanism and regulation of myofilament mechanics and energetics by activator calcium and sarcomere length, as well as contractile protein phosphorylation mediated by protein kinase A. Central to these studies is the question whether such factors impact on muscle function simply by altering thin filament activation state, or whether modulation of cross-bridge cycling also plays a part in the responses of muscle to these stimuli.
authors.affiliation: Department of Physiology and Biophysics, and Cardiovascular Science Program, College of Medicine, University of Illinois, 900 S. Ashland Ave, Chicago, IL 60607-7171, USA. pdetombe@uic.edu
authors.forename: Pieter P
authors.initials: PP
authors.lastname: de Tombe
mesh_terms: D008841:Actin Cytoskeleton / Q000502:physiology*; D000222:Adaptation, Physiological; D002118:Calcium / Q000502:physiology*; D004548:Elasticity; D006321:Heart / Q000502:physiology; D006706:Homeostasis / Q000502:physiology; D040542:Mechanotransduction, Cellular / Q000502:physiology; D020409:Molecular Motor Proteins / Q000502:physiology*; D009200:Myocardial Contraction / Q000502:physiology; D012518:Sarcomeres / Q000502:physiology*; D013314:Stress, Mechanical
chemical_list: D020409:Molecular Motor Proteins; D002118:Calcium