The Study Of Introcellular Signal Transduction Pathway Of PPARγ Inhibiting Myocardial Ecm Remodeling Induced By Angiotensin Ⅱ In Vitro

BackgroundThe extracellular matrix (ECM) in most tissues is composed of a complexarrangement of fibrillar collagen, elastin, microfibrillar proteins, proteoglycans and adhesive proteins such as laminin and fibronectin. Among the extracellular matrix (ECM) proteins, collagens constitute up to 85%. among which type I and type III constitute two-thirds. Fibroblasts are the major source of collagen in the myocardium. Collagen type I accumulation in the heart depends not only on its production, but also on its degradation, which is performed by proteinases, such as matrix metalloproteinase-1 (MMP-1). The activities of MMPs can be specifically inhibited by a family of protease inhibitors, termed tissue inhibitors of matrix metalloproteinases (TIMPs) , which are endogenous physiological inhibitors of MMPs, any aberrant deviation from the delicate balance between MMPs and TIMPs caused by alterations in their activity and regulators, mainly the cytokines may lead to pathological remodeling.So , inhibiting proliferation of cardiac fibroblasts and deposition of collagen are the key of the precaution and reversion of heart remolding and of improving heart function . Peroxisome proliferator-activated receptors (PPAR) are a family of at least 3 nuclear receptors (a, 8, andy). After activation by the ligand, PPARs heterodimerize with retinoic X receptor and recognize PPAR response element which exists in the promoter of target genes. The ligand-activated PPAR functions as a transcription factor and regulates target gene expression. PPARg has been implicated as a mediator of adipocyte differentiation and the mechanism by which...