title: Role of subcellular remodeling in cardiac dysfunction due to congestive heart failure.
abstract: Although alterations in the size and shape of the heart (cardiac remodeling) are considered in explaining cardiac dysfunction during the development of congestive heart failure (CHF), there are several conditions including initial stages of cardiac hypertrophy, where cardiac remodeling has also been found to be associated with either an increased or no change in heart function. Extensive studies have indicated that cardiac dysfunction is related to defects in one or more subcellular organelles such as myofibrils, sarcoplasmic reticulum and sarcolemma, depending upon the stage of CHF. Such subcellular abnormalities in the failing hearts have been shown to occur at both genetic and protein levels. Blockade of the renin-angiotensin system has been reported to partially attenuate changes in subcellular protein, gene expression, functional activities and cardiac performance in CHF. These observations provide support for the role of subcellular remodeling (alterations in molecular and biochemical composition of subcellular organelles) in cardiac dysfunction in the failing heart. On the basis of existing knowledge, it appears that subcellular remodeling during the process of cardiac remodeling plays a major role in the development of cardiac dysfunction in CHF.
authors.affiliation: Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Center and Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
authors.forename: Andrea P
authors.initials: AP
authors.lastname: Babick
authors.forename: Naranjan S
authors.initials: NS
authors.lastname: Dhalla
mesh_terms: D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D015870:Gene Expression; D006333:Heart Failure / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism / Q000648:ultrastructure*; D009210:Myofibrils / Q000378:metabolism / Q000473:pathology / Q000502:physiology; D012084:Renin-Angiotensin System / Q000502:physiology; D012508:Sarcolemma / Q000473:pathology / Q000502:physiology; D012519:Sarcoplasmic Reticulum / Q000473:pathology / Q000502:physiology