文献类型：期刊文献

英文题名：LOX-1 attenuates high glucose-induced autophagy via AMPK/HNF4α signaling in HLSECs

作者：Duan, Qidang[1];Si, Huiling[1];Tian, Limin[3];Zhang, Na[1];Qiu, Jumei[1];Yu, Jing[3];Liu, Jing[3];Zhang, Qi[2]

第一作者：Duan, Qidang

通信作者：Zhang, Q[1];Liu, J[2]

机构：[1]Gansu Univ Chinese Med, Gansu Prov Hosp, Clin Med Coll 1, Lanzhou 730000, Peoples R China;[2]Gansu Prov Hosp, Dept Gerontol, Lanzhou 730000, Peoples R China;[3]Gansu Prov Hosp, Dept Endocrinol, Lanzhou 730000, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Prov Hosp, Dept Gerontol, Lanzhou 730000, Peoples R China;[2]corresponding author), Gansu Prov Hosp, Dept Endocrinol, Lanzhou 730000, Peoples R China.

年份：2022

卷号：8

期号：12

外文期刊名：HELIYON

收录：;Scopus(收录号：2-s2.0-85144806273);WOS:【SCI-EXPANDED(收录号:WOS:000906113700009)】；

基金：Funding Jing Liu was supported by National Natural Science Foundation of China [81760151] . Qi Zhang was supported by National Natural Science Foundation of China [81960173] , National Research Incubation Project of Gansu Pro- vincial People's Hospital [19SYPYB-4] , Lanzhou Health and Wellness Commission [2021005] .

语种：英文

外文关键词：Autophagy; HLSECs; AMPK; HNF4?; LOX-1

摘要：Type 2 diabetes mellitus (T2DM) combined with nonalcoholic fatty liver disease (NAFLD) is a common cause of death. Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is involved in the regulation of autophagy and associated with a variety of diseases, such as atherosclerosis, diabetes, and NAFLD. This study aimed to investigate the effect of LOX-1 on autophagy induced by high glucose levels in human liver sinusoidal endothelial cells (HLSECs) and whether it regulates autophagy through the adenosine monophosphate-activated protein ki-nase/hepatocyte nuclear factor 4 alpha (AMPK/HNF4 alpha) pathway. In this study, HLSECs cultured with high glucose medium showed increased expression of LOX-1, whereas autophagy was inhibited. High glucose levels decreased the AMPK phosphorylation, increased the HNF4 alpha phosphorylation, and retained the HNF4 alpha in the cytoplasm. By contrast, silencing of LOX-1 reversed the phenomenon induced by high glucose levels and restored the HNF4a localization. Taken together, our findings reveal a novel mechanism of high glucose-induced autophagy in HLSECs, namely, the LOX-1-mediated AMPK/HNF4 alpha signaling pathway. Therefore, LOX-1 is an important target molecule for the regulation of autophagy in HLSECs.