ArticleBMC cardiovascular disorders2022
HMGB1 promotes Ox-LDL-induced endothelial cell damage by inhibiting PI3K/Akt signaling pathway.
Article in BMC cardiovascular disorders, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- High-Density Lipoprotein Treatment Effectively Protected the Endothelial Cells, Mitochondria and Myocardium Against Oxidized Low-Density Lipoprotein Damage.Acta Cardiologica Sinica · 2026Article
- miR-330-3p promotes acute coronary syndrome progression via targeting RGS5.Journal of cardiothoracic surgery · 2026Article
- Life-threatening risk factors contribute to the development of diseases with the highest mortality through the induction of regulated necrotic cell death.Cell death & disease · 2025Review
- Endothelial-Protective Actions of Diethylether Extract fromInternational journal of molecular sciences · 2025Article
- Paeonol alleviates ox-LDL-induced endothelial cell injury by targeting the heme oxygenase-1/phosphoinositide 3-kinase/protein kinase B pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Curdione protects vascular endothelial cells and atherosclerosis via the regulation of DNMT1-mediated ERBB4 promoter methylation.Open medicine (Warsaw, Poland) · 2025Article
- Endothelial Dysfunction with Aging: Does Sex Matter?International journal of molecular sciences · 2024Article
- The Role of Alarmins in the Pathogenesis of Atherosclerosis and Myocardial Infarction.Current issues in molecular biology · 2024Review
- MicroRNA-19a-3p inhibits endothelial dysfunction in atherosclerosis by targeting JCAD.BMC cardiovascular disorders · 2024Article
- Higher High-Mobility Group Box-1 Levels are Associated with White Matter Lesions in Ischemic Stroke Patients.Journal of inflammation research · 2023Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAtherosclerosis is the pathological basis of cardio-cerebrovascular diseases. Oxidized low-density lipoprotein (ox-LDL) is an important risk factor for atherosclerosis. Ox-LDL leads to endothelial cell (EC) damage and dysfunction through various processes and promotes the occurrence and deterioration of atherosclerosis. High mobility group box-1 (HMGB1) is a protein associated with cellular damage. In the present study, the effect of HMGB1 on ox-LDL-induced EC damage was determined and the underlying mechanism explored. MATERIALS AND
methodsHuman umbilical vein ECs (HUVECs) were exposed to ox-LDL to induce endothelial damage and changes in HMGB1 expression level were detected using western blotting analysis and reverse transcription-quantitative PCR. To observe the effect of HMGB1 on ox-LDL-induced damage, the HMGB1 expression was downregulated with siRNA, and cell viability, cytotoxicity, and apoptosis rate were assessed. HUVECs were pretreated with LY294002, an inhibitor of the PI3K/Akt pathway, to determine whether the effect of HMGB1 on damage is via the PI3K-Akt pathway.
resultsThe results showed that ox-LDL can upregulate HMGB1 expression in HUVECs and downregulation of HMGB1 expression can prevent ox-LDL-induced damage in HUVECs. Furthermore, the effect of HMGB1 on ox-LDL-induced damage could be promoted by inhibiting the PI3K/Akt signaling pathway.
conclusionThe results indicate HMGB1 may be a promising research target to alleviate ox-LDL-induced EC damage.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.