Role of subcellular remodeling in cardiac dysfunction due to congestive heart failure

被引:10
作者
Babick, Andrea P.
Dhalla, Naranjan S.
机构
[1] St Boniface Gen Hosp, Res Ctr, Inst Cardiovasc Sci, Winnipeg, MB R2H 2A6, Canada
[2] Univ Manitoba, Fac Med, Dept Physiol, Winnipeg, MB, Canada
关键词
myocardial infarction; pressure overload; volume overload; cardiac hypertrophy; cardiac gene expression;
D O I
10.1159/000098358
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
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. Copyright (C) 2007 S. Karger AG, Basel.
引用
收藏
页码:81 / 89
页数:9
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