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非酒精性脂肪性肝炎中的肝纤维化。

Fibrogenesis in nonalcoholic steatohepatitis.

机构信息

Department of Gastroenterology, Polytechnic University of Marche, Ancona, Italy.

出版信息

Expert Rev Gastroenterol Hepatol. 2011 Apr;5(2):179-87. doi: 10.1586/egh.11.28.

DOI:10.1586/egh.11.28
PMID:21476913
Abstract

Nonalcoholic steatohepatitis includes a wide spectrum of liver injury, ranging from simple inflammation to fibrosis and cirrhosis. Whereas simple steatosis has a benign clinical course, steatohepatitis is a recognized cause of progressive liver fibrosis and can develop, in some circumstances, into cirrhosis. The main cause of fibrogenesis is represented by the activation of myofibroblastic cells, which then start to produce matrix filaments. Matrix-producing cells, although mainly constituted of hepatic stellate cells, may have a different origin in the liver. This article will provide information on the sources of matrix-producing cells and the mechanisms involved in the development of fibrogenesis, with particular attention paid to the pathophysiological implications leading from steatohepatitis to fibrosis and cirrhosis.

摘要

非酒精性脂肪性肝炎包括广泛的肝损伤谱,从单纯炎症到纤维化和肝硬化。单纯脂肪变性具有良性的临床过程,而脂肪性肝炎是进行性肝纤维化的公认原因,在某些情况下可发展为肝硬化。纤维发生的主要原因是肌成纤维细胞的激活,然后这些细胞开始产生基质丝。产生基质的细胞虽然主要由肝星状细胞组成,但在肝脏中可能有不同的起源。本文将介绍基质产生细胞的来源和纤维化发展过程中的相关机制,并特别关注从脂肪性肝炎到纤维化和肝硬化的病理生理影响。

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