期刊
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
卷 48, 期 3, 页码 564-569出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2009.06.001
关键词
Mast cells; Matrix metalloproteinases; Oxidative stress; Cardiac fibroblasts; Angiotensin II; Mechanical stretch
资金
- NIH [HL56046]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R29HL056046, R01HL056046] Funding Source: NIH RePORTER
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 IV 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. (C) 2009 Elsevier Ltd. All rights reserved
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