Heart failure, myocardial stunning, and troponin: a key regulator of the cardiac myofilament.
This review discusses post-translational modifications of myofilament regulatory proteins, particularly troponin, associated with heart failure and myocardial stunning--two common disease processes. Altered phosphorylation, partial proteolysis and, possibly, oxidative damage to myofilament proteins may result in abnormalities in both systolic and diastolic function. At a molecular level, these changes may lead to abnormalities in crossbridge cycling and tension development and result in inefficiencies in utilization of energy. Understanding these alterations may lead to new targeted therapies.
Murphy
Anne M
AM
Cardiology Division, Department of Pediatrics, Johns Hopkins University School of Medicine, Ross Building 1144, 720 Rutland Avenue, Baltimore, MD 21205, USA. murphy@jhmi.edu
D008841:Actin Cytoskeleton / Q000502:physiology*; D003971:Diastole / Q000502:physiology; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D009200:Myocardial Contraction / Q000502:physiology*; D017682:Myocardial Stunning / Q000503:physiopathology*; D009206:Myocardium; D013599:Systole / Q000502:physiology; D014336:Troponin / Q000097:blood*
D014336:Troponin