Zoubek Miguel Eugenio, Trautwein Christian, Strnad Pavel
Department of Internal Medicine III, RWTH Aachen University Hospital, Aachen, Germany.
Department of Internal Medicine III, RWTH Aachen University Hospital, Aachen, Germany.
Best Pract Res Clin Gastroenterol. 2017 Apr;31(2):129-141. doi: 10.1016/j.bpg.2017.04.005. Epub 2017 Apr 24.
In chronic liver diseases, an ongoing hepatocellular injury together with inflammatory reaction results in activation of hepatic stellate cells (HSCs) and increased deposition of extracellular matrix (ECM) termed as liver fibrosis. It can progress to cirrhosis that is characterized by parenchymal and vascular architectural changes together with the presence of regenerative nodules. Even at late stage, liver fibrosis is reversible and the underlying mechanisms include a switch in the inflammatory environment, elimination or regression of activated HSCs and degradation of ECM. While animal models have been indispensable for our understanding of liver fibrosis, they possess several important limitations and need to be further refined. A better insight into the liver fibrogenesis resulted in a large number of clinical trials aiming at reversing liver fibrosis, particularly in patients with non-alcoholic steatohepatitis. Collectively, the current developments demonstrate that reversal of liver fibrosis is turning from fiction to reality.
在慢性肝病中，持续的肝细胞损伤与炎症反应共同导致肝星状细胞（HSCs）激活以及细胞外基质（ECM）沉积增加，即肝纤维化。其可进展为肝硬化，特征为实质和血管结构改变以及再生结节的存在。即便在晚期，肝纤维化仍是可逆的，其潜在机制包括炎症环境的转变、活化的肝星状细胞的清除或消退以及细胞外基质的降解。虽然动物模型对于我们理解肝纤维化不可或缺，但它们存在一些重要局限性，需要进一步完善。对肝纤维化形成的更深入了解促成了大量旨在逆转肝纤维化的临床试验，尤其是在非酒精性脂肪性肝炎患者中。总体而言，当前的进展表明肝纤维化的逆转正从虚构变为现实。
