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Extracellular matrix remodeling during the progression of volume overload-induced heart failure Hutchinson KR; Stewart JA Jr; Lucchesi PAJ Mol Cell Cardiol 2010[Mar]; 48 (3): 564-9Volume 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.|Animals[MESH]|Extracellular Matrix/*metabolism[MESH]|Fibroblasts/metabolism[MESH]|Heart Failure/*metabolism[MESH]|Humans[MESH]|Mast Cells/metabolism[MESH]|Matrix Metalloproteinases/metabolism[MESH]|Models, Biological[MESH]|Oxidative Stress/physiology[MESH]|Ventricular Remodeling/physiology[MESH] |
