Understanding post-translational modifications of troponin and other myofilament proteins in heart failure and myocardial stunning may identify new targets for therapy.
Does not support clinical targeting of myofilament PTMs; leaves open new therapeutic avenues pending interventional studies.
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.
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Anne M. Murphy (2006) studied this question.
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