作者: Prakash Ramachandran , John P. Iredale
DOI: 10.1016/J.JHEP.2011.10.026
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摘要: Hepatic fibrosis is the common end point to chronic injury of varied aetiology. There now excellent evidence in both human studies and animal models that liver a bidirectional process with significant reversible component. The hepatic stellate cell (HSC), following activation myofibroblast phenotype, principal producing extracellular matrix (ECM) during fibrogenesis main source TIMP-1, which inhibits endogenous matrix-degrading activity metalloproteinases (MMPs), thus promoting scar deposition. Furthermore, apoptosis activated HSCs critical feature resolution. However, emerging indicates it macrophage master regulator this dynamic fibrogenesis–fibrosis resolution paradigm.