Metabolic Reprogramming in Liver Fibrosis: Focusing on the Metabolic Network of Hepatic Macrophages and Hepatic Stellate Cells

肝纤维化是由慢性肝损伤引发的肝细胞外基质(Extracellular Matrix, ECM)异常沉积和结构紊乱过程，终末可发展为肝硬化(Liver Cirrhosis)和肝细胞癌(Hepatocellular Carcinoma, HCC)。近年研究表明，代谢重编通过重塑肝巨噬细胞(Kupffer细胞/MoMϕs)和肝星状细胞(HSCs)的代谢网络，驱动纤维化进程。本文系统探讨两种关键细胞的代谢特征、互作机制及靶向干预策略，为开发新型抗纤维化疗法提供理论依据。Liver fibrosis is a pathological process characterized by abnormal deposition and structural disorganization of the extracellular matrix (ECM) triggered by chronic liver injury, which can ultimately progress to liver cirrhosis and hepatocellular carcinoma (HCC). Recent studies have demonstrated that metabolic reprogramming drives the fibrogenic process by reshaping the metabolic networks of hepatic macrophages (Kupffer cells/MoMϕs) and hepatic stellate cells (HSCs). This article systematically explores the metabolic characteristics, interaction mechanisms, and targeted intervention strategies of these two key cell types, providing a theoretical foundation for the development of novel anti-fibrotic therapies.