谷氨酰胺转运蛋白ASCT2调控肝星状细胞（HSC）活化和衰老文献综述

摘要：肝星状细胞（Hepatic stellate cells, HSCs）的活化是肝纤维化病理机制的核心环节。

而近年来也认识到，HSC活化是一个高度依赖物质与能量代谢的过程，HSC活化初期发生了代谢重编程。

谷氨酰胺代谢重编程是推动并维持HSC活化更加强有力的因素，目前已将谷氨酰胺的代谢作为干预HSC活化的治疗靶标进行抗肝纤维化药物的研发。

新近研究表明丙氨酸-丝氨酸-半胱氨酸转运载体2（alanineserinecysteine transporter 2, ASCT2）是一种重要的谷氨酰胺特异性的转运载体分子，ASCT2通过其结构特点和生物学作用在谷氨酰胺进入细胞内的吸收以及代谢起着重要的作用。

故本文就HSC活化中谷氨酰胺代谢的作用及ASCT2在谷氨酰胺代谢中的生物学功能等作一综述。

关键词：肝纤维化，肝星状细胞活化，谷氨酰胺代谢，谷氨酰胺转运体，ASCT2Abstract: Activation of hepatic stellate cells (HSCs) is the center of the pathogenesis of liver fibrosis. In recent years, it has also been recognized that HSC activation is a highly dependent process of matter and energy metabolism, and metabolic reprogramming occurs in the early stage of HSC activation. Glutamine metabolism reprogramming is a more powerful factor in promoting and maintaining HSC activation. At present, glutamine metabolism has been developed as a therapeutic target for intervention in HSC activation for anti-hepatic fibrosis drugs. Recent studies have shown that ASCT2 is an important glutamine-specific transporter molecule. ASCT2 plays an important role in the absorption and metabolism of glutamine into cells through its structural characteristics and biological effects. Therefore, this review summarizes the role of glutamine metabolism in HSC activation and the biological function of ASCT2 in glutamine metabolism.Keywords: Hepatic fibrosis, Hepatic stellate cell activation, Glutamine metabolism, Glutamine transporter, ASCT2前言肝纤维化是继发于各种形式慢性肝损伤之后组织修复过程中的代偿反应，也是所有慢性肝病的共同病理过程，其终末阶段将发展为肝硬化、肝衰竭或肝细胞癌。

目前尚无有效治疗肝纤维化的药物，肝纤维化的防治仍是困扰当今医学界的重大难题[1]。

深入研究肝纤维化的发病机制与干预靶标具有重大意义。

现已公认，肝星状细胞（Hepatic stellate cells, HSCs）的活化是肝纤维化病理机制的核心环节[2]。

HSC是肝脏中的间质细胞，又称Ito细胞或储脂细胞。