ArticleAging2021
Azilsartan ameliorates ox-LDL-induced endothelial dysfunction via promoting the expression of KLF2.
Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 23 citations in OpenAlex.
- FTO Deficiency Inhibits Vascular Endothelial Cell Apoptosis and Improved Mitophagy in Obesity-Related Hypertension by Enhancing NDRG1 m6A Methylation.Biochemical genetics · 2026Article
- High-Density Lipoprotein Treatment Effectively Protected the Endothelial Cells, Mitochondria and Myocardium Against Oxidized Low-Density Lipoprotein Damage.Acta Cardiologica Sinica · 2026Article
- Liver sinusoidal endothelial cell fenestrations in metabolic liver disease: from molecular mechanisms to therapeutic perspectives.Cell communication and signaling : CCS · 2026Review
- LDL oxidation and cerebrovascular aging: mechanisms of endothelial dysfunction, inflammation, and vascular cognitive impairment and dementia.Redox biology · 2026Review
- Targeting vascular inflammation and endothelial dysfunction with nanobodies: emerging therapeutic strategies for cardiovascular disease.Frontiers in immunology · 2026Review
- Endothelial dysfunction in cardiovascular diseases: mechanisms and in vitro models.Molecular and cellular biochemistry · 2025Review
- The role of cell junctions in atherosclerosis: implications for inflammation, endothelial dysfunction, and plaque stability.Journal of physiology and biochemistry · 2025Review
- Pharmacological and toxicological roles of Kruppel-like factors (KLFs) in the cardiovascular system: a review.Molecular biology reports · 2025Review
- Rosuvastatin mitigates blood-brain barrier disruption in sepsis-associated encephalopathy by restoring occludin levels.European journal of medical research · 2025Article
- The protective effects of annexin A1 against oxidized-LDL-induced monocytes adhesion to endothelial cells: implication in atherosclerosis.Journal of thrombosis and thrombolysis · 2025Article
- Overexpression of Neural Precursor Cell Expressed Developmentally Downregulated 9 (NEDD9) reduces ox-LDL-induced Anoikis in atherosclerotic vascular endothelial cells.International journal of cardiology. Heart & vasculature · 2025Article
- Cellular senescence in age-related cardiovascular disease: past and future.Frontiers in aging · 2025Review
- Forkhead box P1 transcriptionally activates IGF-1 to lighten ox-LDL-induced endothelial cellular senescence by inactivating NLRP3 inflammasome.Biogerontology · 2024Article
- Article
- Evaluation of the correlation between fetuin-B levels and essential hypertension: a cross-sectional study.Endocrine connections · 2023Article
- Roles of peripheral lipoproteins and cholesteryl ester transfer protein in the vascular contributions to cognitive impairment and dementia.Molecular neurodegeneration · 2023Review
- Curative Effect of AD-MSCs against Cisplatin-Induced Hepatotoxicity in Rats is Potentiated by Azilsartan: Targeting Oxidative Stress, MAPK, and Apoptosis Signaling Pathways.Stem cells international · 2023Article
- Establishment and application of a high-throughput screening model for cell adhesion inhibitors.Frontiers in pharmacology · 2023Article
- The Role of KLF2 in the Regulation of Atherosclerosis Development and Potential Use of KLF2-Targeted Therapy.Biomedicines · 2022Review
- Mechanisms of Oxidized LDL-Mediated Endothelial Dysfunction and Its Consequences for the Development of Atherosclerosis.Frontiers in cardiovascular medicine · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOxidized LDL(Ox-LDL) mediated endothelial dysfunction is involved in the pathogenesis of various cardiovascular diseases, including atherosclerosis. Azilsartan is a potent agent for the treatment of hypertension as the antagonist of the angiotensin II receptor. This study will investigate whether Azilsartan possesses a beneficial effect against endothelial cell dysfunction induced by ox-LDL and explore the underlying preliminary mechanism.
methodsOx-LDL was applied to construct an
resultsFirstly, the elevated expressions of LOX-1, MCP-1, and CXCL-1 induced by stimulation with ox-LDL were significantly suppressed by Azilsartan. The downregulated eNOS and reduced production of NO induced by ox-LDL were reversed by the introduction of Azilsartan. Secondly, enlarged endothelial monolayer permeability and decreased expression of occludin stimulated with ox-LDL were greatly reversed by treatment with Azilsartan but were abolished by silencing the expression of KLF2. Lastly, the inhibited expression of KLF2 induced by ox-LDL was significantly elevated by the introduction of Azilsartan.
conclusionAzilsartan might ameliorate ox-LDL-induced endothelial damage via elevating the expression of KLF2.
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