Role of hepatic stellate cells in fibrogenesis and the reversal of fibrosis
Role of hepatic stellate cells in fibrogenesis and the reversal of fibrosis
复制标题
DOI：
10.1111/j.1440-1746.2006.04658.x
复制
发表时间：
2007-06-01
影响因子：
4.1
通讯作者：
Brenner, David A.
中科院分区：
文献类型：
--
作者：
Kisseleva, Tatiana;Brenner, David A.
肝纤维化是由许多慢性疾病引起的。肝损伤导致胶原生成细胞的激活和细胞外基质蛋白的过度沉积。这一过程是由许多类型的细胞协调的。肝细胞凋亡和炎症细胞刺激促纤维化和促炎症细胞因子的分泌，如转化生长因子-β1、血管紧张素II、瘦素，进而激活I型胶原的主要来源肝星状细胞。本文就肝纤维化发病机制的最新研究进展作一综述。
Liver fibrosis is caused by many chronic diseases. Liver injury results in activation of collagen-producing cells and excessive deposition of extracellular matrix proteins. This process is orchestrated by many cell types. Hepatocytes apoptosis and inflammatory cells trigger secretion of profibrogenic and proinflammatory cytokines, such as transforming growth factor-beta 1, angiotensin II, leptin, which in turn activates hepatic stellate cells, the major source of collagen type I. This review is focused on recent progress in the study of the pathogenesis of liver fibrosis.