LOX-1 promotes hypoxia-induced autophagy and apoptosis in endo-thelial cells
10.12092/j.issn.1009-2501.2025.08.002
- VernacularTitle:LOX-1促进低氧诱导的内皮细胞自噬与凋亡
- Author:
Yanfei LI
1
;
Can HUANG
;
Ping LUO
;
Fang HE
;
Changping HU
Author Information
1. 中南大学湘雅医学院附属长沙医院,长沙市第一医院,药剂科,长沙 410005,湖南
- Publication Type:Journal Article
- Keywords:
lectin-like oxidized low-density lipo-protein receptor-1;
hypoxia;
autophagy;
apoptosis;
endothelial cell
- From:
Chinese Journal of Clinical Pharmacology and Therapeutics
2025;30(8):1017-1025
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the role of lectin-like oxidized low-density lipoprotein receptor-1(LOX-1)in hypoxia-induced autophagy and apopto-sis in endothelial cells.METHODS:Human umbili-cal vein endothelial cells(HUVECs)were exposed to hypoxia(1％O2)for varying durations(0,6,12,24 h)to evaluate autophagy and apoptosis levels.LOX-1 was further intervened to explore its effects on autophagy and apoptosis.GFP-LC3B adenovirus in-fection was observed under fluorescence microsco-py to assess LC3B expression.Autophagosomes were detected by transmission electron microscopy(TEM).LOX-1 mRNA levels were measured using re-al-time PCR.Protein expression of LOX-1,LC3Ⅱ/Ⅰ,Beclin-1,Atg5,cleaved-caspase 3,Bax,and Bcl-2 was analyzed by Western blot.Reactive oxygen spe-cies(ROS)levels were quantified using the DCFH-DA fluorescent probe.Apoptosis was assessed via Hoechst staining and flow cytometry(Annexin V-PI double staining).RESULTS:Hypoxia(1％O2,24 h)significantly increased LC3Ⅱ puncta under fluores-cence microscopy,upregulated LC3Ⅱ/Ⅰ protein ex-pression,and induced autophagosome formation observed by TEM.Hypoxia elevated ROS produc-tion and promoted apoptosis.LOX-1 mRNA and protein expression were upregulated in hypoxic HU-VECs.LOX-1 siRNA intervention markedly reversed hypoxia-induced autophagy,downregulating au-tophagy-related proteins(Beclin-1,Atg5,LC3Ⅱ/Ⅰ).LOX-1 siRNA also suppressed ROS generation and inhibited apoptosis,as evidenced by decreased ex-pression of cleaved-caspase 3 and Bax,and in-creased Bcl-2 levels.CONCLUSION:Hypoxia in-duced upregulation of LOX-1 expression to produce ROS,thereby promoting autophagy and apoptosis in endothelial cells.
