Extracellular matrix remodeling during the progression of volume overload-induced heart failure.
Extracellular matrix remodeling during the progression of volume overload-induced heart failure.
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DOI：
10.1016/j.yjmcc.2009.06.001
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发表时间：
2010-03
影响因子：
5
通讯作者：
Lucchesi, Pamela A.
中科院分区：
文献类型：
--
作者：
Hutchinson, Kirk R.;Stewart, James A., Jr.;Lucchesi, Pamela A.
关键词：
容量超负荷导致的心力衰竭导致以心腔扩张、离心性心肌细胞肥大和细胞外基质(ECM)重塑改变为特征的进行性左室重塑。ECM基质支架是心肌结构完整性的重要决定因素，并积极参与跨室壁的力传递。作为对这种血流动力学过载的反应，ECM经历了不同于压力过载的独特的重塑模式。ECM曾经被认为是一个静态的实体，现在被认为是一种高度适应性的结构，它受到机械应激、神经激素激活、炎症和氧化应激的动态调节，导致胶原和其他基质成分的变化，以及基质金属蛋白酶(MMPs)表达和激活的净变化。这些变化决定了在批量过载听到故障过程中ECM的总体周转率。这篇综述将讨论在心脏病进展过程中细胞和分子机制决定细胞外基质重塑的时间模式。
Volume overload-induced heart failure results in progressive left ventricular remodeling characterized by chamber dilation, eccentric cardiac myocyte hypertrophy and changes in extracellular matrix (ECM) remodeling changes. The ECM matrix scaffold is an important determinant of the structural integrity of the myocardium and actively participates in force transmission across the LV wall. In response to this hemodynamic overload, the ECM undergoes a distinct pattern of remodeling that differs from pressure overload. Once thought to be a static entity, the ECM is now regarded to be a highly adaptive structure that is dynamically regulated by mechanical stress, neurohormonal activation, inflammation and oxidative stress, that result in alterations in collagen and other matrix components and a net change in matrix metalloproteinase (MMP) expression and activation. These changes dictate overall ECM turnover during volume overload hear failure progression. This review will discuss the cellular and molecular mechanisms that dictate the temporal patterns of ECM remodeling during heart disease progression.
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3.5
作者：
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