ArticleJournal of cellular and molecular medicine2010
Effect of irreversibly glycated LDL in human vascular smooth muscle cells: lipid loading, oxidative and inflammatory stress.
Article in Journal of cellular and molecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 72 citations in OpenAlex.
- Review
- [Buffering effect of intensive lipid lowering on mortality risk in type 2 diabetic patients with chronic kidney disease and challenging glycemic management: a cohort study based on dual metabolic trajectories].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Overstretch causes lipid accumulation in vascular smooth muscle cells dependent on NADPH oxidase 1.Mechanobiology in medicine · 2025Article
- Advanced glycation end product-modified low-density lipoprotein promotes pro-osteogenic reprogramming via RAGE/NF-κB pathway and exaggerates aortic valve calcification in hamsters.Molecular medicine (Cambridge, Mass.) · 2024Article
- Article
- Nox4 as a novel therapeutic target for diabetic vascular complications.Redox biology · 2023Review
- The Role of Advanced Glycation End Products on Dyslipidemia.Metabolites · 2023Review
- Cardiovascular Dysfunction in Intrauterine Growth Restriction.Current hypertension reports · 2022Review
- Role of Endothelial Regeneration and Overloading of Enterocytes with Lipids in Capturing of Lipoproteins by Basement Membrane of Rat Aortic Endothelium.Biomedicines · 2022Article
- Development and validation of a risk prediction nomogram for in-stent restenosis in patients undergoing percutaneous coronary intervention.BMC cardiovascular disorders · 2021Observational
- Article
- Article
- Endothelial Dysfunction in Diabetes Is Aggravated by Glycated Lipoproteins; Novel Molecular Therapies.Biomedicines · 2020Review
- Differential Regulation of mTOR Complexes with miR-302a Attenuates Myocardial Reperfusion Injury in Diabetes.iScience · 2020Article
- Targeting oxidative stress and anti-oxidant defence in diabetic kidney disease.Journal of nephrology · 2020Review
- Hypertension accelerates age-related intrarenal small artery (IRSA) remodelling and stiffness in rats with possible involvement of AGEs and RAGE.Histology and histopathology · 2020Article
- c-Kit suppresses atherosclerosis in hyperlipidemic mice.American journal of physiology. Heart and circulatory physiology · 2019Article
- The phosphatase activity of soluble epoxide hydrolase regulates ATP-binding cassette transporter-A1-dependent cholesterol efflux.Journal of cellular and molecular medicine · 2019Article
- Myocardial Ischemia and Diabetes Mellitus: Role of Oxidative Stress in the Connection between Cardiac Metabolism and Coronary Blood Flow.Journal of diabetes research · 2019Review
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The major complication of diabetes is accelerated atherosclerosis, the progression of which entails complex interactions between the modified low-density lipoproteins (LDL) and the cells of the arterial wall. Advanced glycation end product-modified-LDL (AGE-LDL) that occurs at high rate in diabetes contributes to diabetic atherosclerosis, but the underlying mechanisms are not fully understood. The aim of this study was to assess the direct effect of AGE-LDL on human vascular smooth muscle cells (hSMC) dysfunction. Cultured hSMC incubated (24 hrs) with human AGE-LDL, native LDL (nLDL) or oxidized LDL (oxLDL) were subjected to: (i) quantification of the expression of the receptors for modified LDL and AGE proteins (LRP1, CD36, RAGE) and estimation of lipid loading, (ii) determination of NADPH oxidase activity and reactive oxygen species (ROS) production and (iii) evaluation of the expression of monocyte chemoattractant protein-1 (MCP-1). The results show that exposure of hSMC to AGE-LDL (compared to nLDL) induced: (a) increased NADPH oxidase activity (30%) and ROS production (28%) by up-regulation of NOX1, NOX4, p22phox and p67phox expression, (b) accumulation of intracellular cholesteryl esters, (c) enhanced gene expression of LRP1 (160%) and CD36 (35%), and protein expression of LRP1, CD36 and RAGE, (d) increased MCP-1 gene expression (160%) and protein secretion (300%) and (e) augmented cell proliferation (30%). In conclusion, AGE-LDL activates hSMC (increasing CD36, LRP1, RAGE), inducing a pro-oxidant state (activation of NADPHox), lipid accumulation and a pro-inflammatory state (expression of MCP-1). These results may partly explain the contribution of AGE-LDL and hSMC to the accelerated atherosclerosis in diabetes.
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