转运蛋白调控的分子机制及其在肝内胆汁淤积中的损害

Xiping Li, Y. Zu, Guodong Li, Dong Xiang, Chengliang Zhang, Dong Liu
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引用次数: 1

摘要

肝内胆汁淤积症(IC)是由于肝细胞和/或胆汁毛细血管结构和功能异常而引起的胆汁形成和排泄障碍引起的一种肝脏疾病。IC通常由肝炎病毒、饮酒、药物性肝损伤、自身免疫性肝病和遗传引起。在缺乏有效治疗的情况下,IC可发展为肝纤维化、肝硬化并最终导致肝功能衰竭。然而,IC背后的机制仍然知之甚少。IC被认为与肝细胞转运蛋白的转录、功能和定位的变化密切相关。为了更好地了解IC中转运蛋白的分子机制,本文综述了这些转运蛋白在IC中的作用,并讨论了它们在IC中的潜在调控机制,旨在为了解IC的发病机制和开发有效的药物治疗提供参考。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Molecular mechanisms of transporter regulation and their impairment in intrahepatic cholestasis
Intrahepatic cholestasis (IC) is a liver disease caused by disorders in bile formation and excretion, owing to structural and functional abnormalities in hepatocytes and/or bile capillaries. IC is commonly caused by hepatitis virus, alcohol consumption, drug-induced liver damage, autoimmune liver disease and heredity. In the absence of effective treatment, IC can progress to liver fibrosis, cirrhosis and ultimately liver failure. However, the mechanisms underlying IC remain poorly understood. IC is believed to be closely associated with changes in the transcription, function and localization of hepatocellular transport proteins. To better understand the molecular mechanisms of transport proteins in IC, herein, we review the roles of these transport proteins and discuss their underlying regulatory mechanisms in IC. Our aim is to provide a reference for understanding IC pathogenesis and developing effective drug therapies.
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