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胆道闭锁肝纤维化研究进展 预览 被引量:9

Advances in the research of liver fibrosis in biliary atresia
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摘要 胆道闭锁(BA)是严重危及婴幼儿生命健康的消化系统疾病之一,晚期肝脏纤维化是导致患儿死亡的主要原因。在胆道闭锁发病过程中,病毒感染可诱导一系列免疫和炎症反应,导致调节性T细胞(Treg细胞)减少,CD14表达增高,多种炎症通路以及转化生长因子-β(TGF-β)/Smad2/3促纤维化通路被激活。激活的通路产生大量炎性介质损伤肝细胞和胆管细胞,释放各种促炎因子、氧代谢产物和细胞因子,进一步加重肝、胆系统损伤造成肝细胞内环境失衡,失衡的内环境伴随肝实质细胞、肝巨噬细胞、肝内聚集的炎性细胞等发生适应性变性、坏死、增生,导致肝星形细胞(HSCs)激活,HSCs转化为成纤维细胞,促进肝纤维化进程。免疫、炎症损伤、促纤维化通路是导致胆道闭锁肝纤维化肝硬化的三大重要因素。 Biliary atresia (BA) is one of the most serious digestive system diseases, which threatens the health of infants. Liver fibrosis is a major cause of death in children with BA. In the process of the pathogenesis of BA, virus infection can in?duce a series of immune and inflammatory reaction, result in a decrease of regulatory T cells (Treg cells) and high expression of CD14, activating a variety of inflammatory pathways and TGF-β/Smad2/3 pro-fibrogenic pathway, which produces a large number of medium damage of liver cells and bile duct cells, releases proinflammatory factor, oxygen metabolism matter and cytokines. These changes further aggravate damage of hepatobiliary system and cause the internal environment imbalance of liver parenchyma cells. The imbalance of internal environment with adaptive degeneration and necrosis in liver parenchyma cells, hepatic macrophages and gathered inflammatory cells leads to the activation of hepatic stellate cells (HSCs). HSCs can be converted into fibroblast cells, and promote the process of liver fibrosis. Immune and inflammatory lesions, pro-fibrogenic pathway are the important factors in contributing to liver fibrosis and cirrhosis of biliary atresia.
作者 丁美云 詹江华 DING Meiyun, ZHAN Jianghua (1 The Graduate School of Tianfin Medical University, Tianfin 300070, China; 2 Tianfin Children's Hospital)
出处 《天津医药》 CAS 2015年第1期4-7,共4页 Tianjin Medical Journal
基金 天津市卫计委重点攻关项目(14KG129)
关键词 胆道闭锁 肝硬化 T淋巴细胞 调节性 转化生长因子Β 抗原 CDL4 SMAD蛋白质类 biliary atresia liver cirrhosis T-lymphocytes,regulatory transforming growth factor beta Smad proteins
作者简介 丁美云(1988),女,硕士在读,主要从事小儿普通外科、胆道闭锁方面研究。 通讯作者及审校者zhanjianghuatj@ 163.com
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