Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease. Non-alcoholic steatohepatitis (NASH) is a more severe form of NAFLD and causes subsequent pathological changes including cirrhosis and hepatocellular carcinoma. Inflammation is the key pathological change in NASH and involves a series of cytokines and chemokines. The C-X-C motif chemokine 10 (CXCL10), which is known as a pro-inflammation chemokine, was recently proven to play a pivotal role in the pathogenesis of NASH. Hepatic CXCL10 is mainly secreted by hepatocytes and liver sinusoidal endothelium. By binding to its specific receptor CXCR3, CXCL10 recruits activated CXCR3+T lymphocytes and macrophages to parenchyma and promotes inflammation, apoptosis and fibrosis. The circulating CXCL10 level correlates with the severity of lobular inflammation and is an independent risk factor for NASH patients. Thus, CXCL10 may be both a potential prognostic tool and a therapeutic target for the treatment of patients with NASH. The aim of this review is to highlight the growing advances in basic knowledge and clinical interest of CXCL10 in NASH to propagate new insights into novel pharmacotherapeutic avenues.

中文翻译：

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非酒精性脂肪性肝炎中的 CXC 基序趋化因子 10：作为促炎因子的作用和临床意义

非酒精性脂肪性肝病 (NAFLD) 是慢性肝病的最常见原因。非酒精性脂肪性肝炎 (NASH) 是一种更严重的 NAFLD，会导致随后的病理变化，包括肝硬化和肝细胞癌。炎症是NASH的关键病理变化，涉及一系列细胞因子和趋化因子。CXC 基序趋化因子 10 (CXCL10) 被称为促炎症趋化因子，最近被证明在 NASH 的发病机制中起关键作用。肝CXCL10主要由肝细胞和肝窦内皮分泌。通过与其特异性受体 CXCR3 结合，CXCL10 招募激活的 CXCR3+T淋巴细胞和巨噬细胞进入实质并促进炎症、细胞凋亡和纤维化。循环 CXCL10 水平与小叶炎症的严重程度相关，是 NASH 患者的独立危险因素。因此，CXCL10 可能既是一种潜在的预后工具，也是治疗 NASH 患者的治疗靶点。本综述的目的是强调 CXCL10 在 NASH 中的基础知识和临床兴趣方面的不断进步，以传播对新药物治疗途径的新见解。