肝损伤与肝肌成纤维细胞的激活
Liver Injury and the Activation of the Hepatic Myofibroblasts.
作者信息
Jiang Joy X, Török Natalie J
机构信息
Department of Internal Medicine, Division of Gastroenterology and Hepatology, UC Davis Medical Center, Sacramento, CA.
出版信息
Curr Pathobiol Rep. 2013 Sep 1;1(3):215-223. doi: 10.1007/s40139-013-0019-6.
Abstract
Liver fibrosis is a wound healing process, the end result of chronic liver injury elicited by different noxious stimuli. Activated hepatic stellate cells or myofibroblasts and portal myofibroblasts are considered as the main producers of the extracellular matrix in the liver. Upon liver injury the quiescent stellate cells transdifferentiate into myofibroblasts a process highlighted by the loss of vitamin A stores, upregulation of interstitial type collagens, smooth muscle α actin, matrix metalloproteinases, proteoglycans, and the induction of cell survival pathways. Activation of hepatic stellate cells is a result of a complex interplay between the parenchymal cells, immune cells, extracellular matrix mechanics and extrahepatic milieu such as the gut microbiome. In this review we will focus on the pathomechanism of stellate cell activation following chronic liver injury; with the aim of identifying possible treatment targets for anti-fibrogenic agents.
摘要
肝纤维化是一种伤口愈合过程，是由不同有害刺激引发的慢性肝损伤的最终结果。活化的肝星状细胞或肌成纤维细胞以及门静脉肌成纤维细胞被认为是肝脏细胞外基质的主要产生者。肝脏损伤时，静止的星状细胞转分化为肌成纤维细胞，这一过程的特征是维生素A储存丧失、间质型胶原蛋白、平滑肌α肌动蛋白、基质金属蛋白酶、蛋白聚糖上调，以及细胞存活途径的诱导。肝星状细胞的活化是实质细胞、免疫细胞、细胞外基质力学和肝外环境（如肠道微生物群）之间复杂相互作用的结果。在本综述中，我们将聚焦于慢性肝损伤后星状细胞活化的发病机制；目的是确定抗纤维化药物可能的治疗靶点。
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