Kim Moon Young
Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea.
Korean J Gastroenterol. 2017 Jun 25;69(6):341-347. doi: 10.4166/kjg.2017.69.6.341.
Understanding the pathogenesis of non-alcoholic steatohepatitis (NASH) and its fibrosis progression is still evolving. Nonetheless, current evidence suggests that mechanisms involved are very complex parallel processes with multiple metabolic factors. Lipotoxicity related with excess saturated free fatty acids, obesity, and insulin resistance acts as the central driver of cellular injury via oxidative stress. Hepatocyte apoptosis and/or senescence are also contribute to the activation of inflammasome via various intra- and inter-cellular signaling mechanisms that lead to fibrosis. Current evidence suggests that periportal components, including ductular reaction and expansion of the hepatic progenitor cell compartment, may be involved and that the T-helper 17 cell response may mediate disease progression. This review aims to provide a brief overview of the pathogenesis of NASH and fibrosis progression from inflammation to fibrosis.
对非酒精性脂肪性肝炎（NASH）的发病机制及其纤维化进展的理解仍在不断发展。尽管如此，目前的证据表明，所涉及的机制是非常复杂的并行过程，涉及多种代谢因素。与过量饱和游离脂肪酸、肥胖和胰岛素抵抗相关的脂毒性通过氧化应激成为细胞损伤的主要驱动因素。肝细胞凋亡和/或衰老也通过各种细胞内和细胞间信号机制促进炎性小体的激活，进而导致纤维化。目前的证据表明，包括小胆管反应和肝祖细胞区室扩张在内的汇管区成分可能参与其中，并且辅助性T细胞17细胞反应可能介导疾病进展。本综述旨在简要概述NASH的发病机制以及从炎症到纤维化的纤维化进展。
