Department of Hepatobiliary Surgery, Xi-Jing Hospital, The Fourth Military Medical University, Xi'an, China.
Front Immunol. 2022 Jun 28;13:936196. doi: 10.3389/fimmu.2022.936196. eCollection 2022.
Chronic liver injury can be caused by many factors, including virus infection, alcohol intake, cholestasis and abnormal fat accumulation. Nonalcoholic steatohepatitis (NASH) has become the main cause of liver fibrosis worldwide. Recently, more and more evidences show that hepatic microenvironment is involved in the pathophysiological process of liver fibrosis induced by NASH. Hepatic microenvironment consists of various types of cells and intercellular crosstalk among different cells in the liver sinusoids. Liver sinusoidal endothelial cells (LSECs), as the gatekeeper of liver microenvironment, play an irreplaceable role in the homeostasis and alterations of liver microenvironment. Many recent studies have reported that during the progression of NASH to liver fibrosis, LSECs are involved in various stages mediated by a series of mechanisms. Therefore, here we review the key role of crosstalk between LSECs and hepatic microenvironment in the progression of NASH to liver fibrosis (steatosis, inflammation, and fibrosis), as well as promising therapeutic strategies targeting LSECs.
慢性肝损伤可由多种因素引起，包括病毒感染、饮酒、胆汁淤积和脂肪异常堆积。非酒精性脂肪性肝炎（NASH）已成为全球范围内肝纤维化的主要病因。最近越来越多的证据表明，肝微环境参与了 NASH 诱导的肝纤维化的病理生理过程。肝微环境由肝窦内各种类型的细胞和细胞间的相互作用组成。肝窦内皮细胞（LSEC）作为肝微环境的守门员，在肝微环境的稳态和改变中发挥着不可替代的作用。许多最近的研究报道称，在 NASH 向肝纤维化进展的过程中，LSEC 通过一系列机制参与了多个阶段。因此，我们在这里综述了 LSEC 与肝微环境之间的相互作用在 NASH 向肝纤维化（脂肪变性、炎症和纤维化）进展中的关键作用，以及针对 LSEC 的有前途的治疗策略。
