Cardiac myocyte remodeling in hypertrophy and progression to failure
Cardiac myocyte remodeling in hypertrophy and progression to failure
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DOI：
10.1054/jcaf.2002.129280
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发表时间：
2002-12-01
影响因子：
6
通讯作者：
Gerdes, AM
中科院分区：
文献类型：
--
作者：
Gerdes, AM
收缩的肌细胞大小变化很大，形状通常类似于椭圆形。尽管它们在室壁内的排列相当复杂，但它们的长度是切线的，横轴是跨壁的。因此，很多年前就有人提出，心肌细胞长度的改变(L)可能有助于腔内扩张，而心肌细胞的横向生长可能是心肌肥厚时室壁增厚的主要原因。近年来，更有效、更全面、更精确地测量心肌细胞尺寸的方法的发展证实了这一点。具体地说，代偿期的压力超负荷导致以心肌细胞横截面积(CSA)增加为特征的向心性肥大。补偿阶段的体积过载导致燃烧室直径/壁厚成比例增加，其特征是L和CsA增加。肌细胞过度延长(肌节连续增加)而CsA没有进一步改变，这似乎是导致房室扩张进展到失败的主要细胞改变。这一事件发生在出现症状性心力衰竭之前很久。了解和定位这种细胞变化背后的相关异常信号应该会有相当大的临床后果。
Contracting myocytes are highly variable in size and generally resemble elliptical cylinders in shape. Although their arrangement within the ventricular wall is rather complex, their length runs in a tangential manner, and their transverse axis runs transmurally. Consequently, it was proposed many years ago that changes in myocyte length (L) may contribute to chamber dilatation while myocyte transverse growth may be largely responsible for wall thickening during cardiac hypertrophy. In recent years, the development of more efficient, comprehensive, and precise methods of measuring cardiac myocyte dimensions has confirmed this. Specifically, pressure overloading during the compensated phase leads to concentric hypertrophy, which is characterized by an increase in myocyte cross-sectional area (CSA). Volume overloading during the compensated phase leads to a proportional increase in chamber diameter/wall thickness, which is characterized by increased L and CSA. Excessive myocyte lengthening (from series sarcomere addition) without a further change in CSA, appears to be the primary cellular alteration leading to chamber dilatation in the progression to failure. This event occurs long before the development of symptomatic heart failure. Understanding and targeting the associated abnormal signaling underlying this cellular change should have considerable clinical consequences.