β淀粉样蛋白假说在肝纤维化相关疾病中的研究进展  

Research Progress of AmyloidβHypothesis in Liver Fibrosis Related Diseases

作　　者：吕鸿宇 王斌[1] LYU Hongyu;WANG Bin(Department Two of General Surgery,Shenzhen Children′s Hospital Affiliated to China Medical University,Shenzhen 518000,China)

机构地区：[1]中国医科大学附属深圳市儿童医院普外二科,广东深圳518000

出　　处：《医学综述》2023年第21期4428-4432,共5页Medical Recapitulate

基　　金：国家自然科学基金(81770512);广东省高水平医院建设专项经费资助(深儿医科教〔2022〕28号);深圳市医疗卫生三名工程项目(SZSM201812055)。

摘　　要：β淀粉样蛋白(Aβ)聚集形成的淀粉样斑块是阿尔茨海默病的主要病理特征之一。肝脏作为神经Aβ的最主要清除器官,主要通过低密度脂蛋白受体1、载脂蛋白E、晚期糖基化终末产物受体及高密度脂蛋白受体等介质实现对Aβ的摄入和降解。在非酒精性脂肪性肝病、代偿期肝硬化、胆管闭锁等肝纤维化相关疾病中亦可发现Aβ代谢异常,Aβ沉积可促进疾病的病理进程,但具体机制目前尚未完全阐明。因此,降低Aβ的负荷或可成为肝纤维化相关疾病的治疗靶点。Amyloid-β(Aβ)plaques formed by the aggregation of amyloid-βoligomers are one of the main pathological features of Alzheimer′s disease.As the most important organ clearing Aβnervous,the liver mainly completes the uptake and degradation of Aβthrough mediators such as low-density lipoprotein receptor 1,apolipoprotein E,advanced glycosylation end-product receptor and high-density lipoprotein receptor.The abnormalities in Aβmetabolism can also be found in liver fibrosis-related diseases including nonalcoholic fatty liver disease,compensated cirrhosis,and biliary atresia,and its deposition promotes the pathological process of the disease,but the specific mechanism has not yet been fully elucidated.Therefore,reducing the burden of Aβmay be used as a therapeutic target for liver fibrosis-related diseases.

关 键 词：肝纤维化相关疾病 Β淀粉样蛋白 血浆标志物 

分 类 号：R657.3[医药卫生—外科学]