血红素加氧酶1对肝缺血再灌注损伤的细胞保护机制进展  

Advances in Cytoprotective Mechanisms of Heme Oxygenase 1 to Hepatic Ischemia-reperfusion Injury

作　　者：杨轶涵 展希[1] 方育[1] YANG Yihan;ZHAN Xi;FANG Yu(Department of Anesthesiology,the First Affiliated Hospital of Kunming Medical University,Kunming 650032,China)

机构地区：[1]昆明医科大学第一附属医院麻醉科,昆明650032

出　　处：《医学综述》2022年第14期2733-2738,共6页Medical Recapitulate

基　　金：云南省科技厅-昆医联合专项(202001AY070001-041)。

摘　　要：肝缺血再灌注损伤(HIRI)包括缺血损伤和循环恢复后的再灌注损伤两个过程,是肝切除、肝移植等术后发生肝功能障碍甚至肝衰竭的重要原因。血红素加氧酶1(HO-1)是一种重要的内源性细胞保护基因,其能作用于肝脏的实质细胞和非实质细胞(库普弗细胞、肝窦内皮细胞等),并通过复杂的分子信号通路相互交联发挥保护作用。目前针对HIRI治疗的效果尚不理想,随着精准医疗的快速发展,了解HO-1在HIRI中的细胞保护机制对未来的肝细胞靶向治疗极为重要。Hepatic ischemia-reperfusion injury(HIRI)includes ischemia damage and reperfusion injury after circulation recovery,which is an important cause of liver dysfunction and even liver failure after liver resection,liver transplantation and other surgeries.Heme oxygenase 1(HO-1)is an important endogenous cell protection gene in the body,which can act on hepatic parenchymal cells and non-parenchymal cells including Kupffer cells and hepatic sinusoidal endothelial cells,etc.,which play a protective role through cross-linking of complex molecular signaling pathways.Current treatments for HIRI are not ideal,and with the rapid development of precision medicine,it is important to understand the cytoprotective mechanisms of HO-1 in HIRI for future hepatocyte targeted therapies.

关 键 词：肝缺血再灌注损伤 血红素加氧酶1 库普弗细胞 肝窦内皮细胞 

分 类 号：R333.4[医药卫生—人体生理学]