文献类型：期刊文献

英文题名：LOX-1 silencing activates the PI3K/AKT pathway to inhibit ox-LDL-induced apoptosis of THVECs

作者：Wang, Shuyue[1];Ding, Weiwen[1];Cheng, Rangbao[1];Wei, Lirong[1];Tian, Qianqian[1];Zhu, Junyi[1];Li, Yingying[1];Zhang, Qi[1,2]

第一作者：王世勇;王生瑜

通信作者：Zhang, Q[1]

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

年份：2026

卷号：784

外文期刊名：ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS

收录：;Scopus(收录号：2-s2.0-105044798189);WOS:【SCI-EXPANDED(收录号:WOS:001827054100001)】；

基金：Finances Qi Zhang received funding from the Research on the Comprehensive Prevention and Control System and Key Technologies of Osteoporosis in Gansu Province [22YF7FA096] and the National Natural Science Foundation of China [81960173] .

语种：英文

外文关键词：LOX-1; Type H bone vascular endothelial cells; Diabetic osteoporosis; PI3K/AKT; Apoptosis

摘要：Objective: This study aimed to investigate the mechanism by which the LOX-1/PI3K/AKT signaling axis regulates oxidized low-density lipoprotein (ox-LDL)-induced apoptosis in type H bone vascular endothelial cells (THVECs). Methods: Primary THVECs were isolated from rat trabecular bone and identified via coimmunofluorescence staining for CD31 and endomucin (EMCN). The cells were divided into four groups: control, ox-LDL (100 mu g/mL), ox-LDL + LV (lentiviral LOX-1 knockdown), and ox-LDL + CON (LV-control). Additionally, an AKT inhibitor (MK-2206) was used to verify the role of PI3K/AKT signaling. Western blotting (WB) was used to measure the protein levels of LOX-1, PI3K, phosphorylated PI3K (p-PI3K), AKT, phosphorylated AKT (p-AKT), Bax,Cleavedcaspse 3,BMP2 and OPN. Flow cytometry was used to detect apoptosis rate and ROS (Reactive Oxygen Species) levels. Results: ox-LDL treatment significantly induced apoptosis in THVECs cells, upregulated the expression of LOX-1 and apoptoic proteins, promoted reactive oxygen species production, impaired bone remodeling, and reduced the phosphorylation levels of PI3K and AKT. Lentivirus-mediated LOX-1 knockdown reversed ox-LDL-induced endothelial dysfunction and promoted angiogenesis. Conclusion: ox-LDL induces the silencing of the LOX-1 pathway, activates the PI3K/AKT pathway, promots apoptosis, and affects bone remodeling and angiogenesis. This suggests that targeting LOX-1 may become a potential strategy for the treatment of diabetic osteoporosis.