Babick Andrea P, Dhalla Naranjan S
Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Center and Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
Med Princ Pract. 2007;16(2):81-9. doi: 10.1159/000098358.
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.
虽然在解释充血性心力衰竭(CHF)发展过程中的心脏功能障碍时会考虑心脏大小和形状的改变(心脏重塑),但存在多种情况,包括心脏肥大的初始阶段,在这些阶段也发现心脏重塑与心脏功能增加或无变化有关。广泛的研究表明,根据CHF的阶段,心脏功能障碍与一个或多个亚细胞器(如肌原纤维、肌浆网和肌膜)的缺陷有关。衰竭心脏中的这种亚细胞异常已在基因和蛋白质水平上被证实存在。据报道,肾素-血管紧张素系统的阻断可部分减轻CHF中亚细胞蛋白质、基因表达、功能活动和心脏性能的变化。这些观察结果支持亚细胞重塑(亚细胞器分子和生化组成的改变)在衰竭心脏心脏功能障碍中的作用。基于现有知识,似乎心脏重塑过程中的亚细胞重塑在CHF心脏功能障碍的发展中起主要作用。