ArticleBioMed research international2015
Ox-LDL induces dysfunction of endothelial progenitor cells via activation of NF-κB.
Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- MiR-582-3p regulates endothelial cell function in lower extremity deep vein thrombosis by targeting TFRC.Annals of hematology · 2026Article
- Upregulation of IL-32γ in endothelial cells promotes macrophage recruitment and inflammatory progression in atherosclerosis.Scientific reports · 2026Article
- Molecular Interplay between hypertension and dyslipidemia in cardiovascular pathogenesis: toward precision-based therapeutic strategies.Frontiers in cardiovascular medicine · 2026Review
- Lycopene inhibits pyroptosis of endothelial progenitor cells induced by ox-LDL through the AMPK/mTOR/NLRP3 pathway.Open medicine (Warsaw, Poland) · 2024Article
- Atherosclerosis and Toll-Like Receptor4 (TLR4), Lectin-Like Oxidized Low-Density Lipoprotein-1 (LOX-1), and Proprotein Convertase Subtilisin/Kexin Type9 (PCSK9).Mediators of inflammation · 2024Review
- The Potential Role of Connexins in the Pathogenesis of Atherosclerosis.International journal of molecular sciences · 2023Review
- Small Molecule BRD4 Inhibitors Apabetalone and JQ1 Rescues Endothelial Cells Dysfunction, Protects Monolayer Integrity and Reduces Midkine Expression.Molecules (Basel, Switzerland) · 2022Article
- New insight into dyslipidemia-induced cellular senescence in atherosclerosis.Biological reviews of the Cambridge Philosophical Society · 2022Review
- Impact of Non-Pharmacological Interventions on the Mechanisms of Atherosclerosis.International journal of molecular sciences · 2022Review
- The Role of Endothelial Progenitor Cells in Atherosclerosis and Impact of Anti-Lipemic Treatments on Endothelial Repair.International journal of molecular sciences · 2022Review
- ox-LDL-Induced Endothelial Progenitor Cell Oxidative Stress via p38/Keap1/Nrf2 Pathway.Stem cells international · 2022Article
- Molecular mechanisms of endothelial dysfunction in Kawasaki-disease-associated vasculitis.Frontiers in cardiovascular medicine · 2022Review
- Endothelial progenitor cells and coronary artery disease: Current concepts and future research directions.World journal of clinical cases · 2021Review
- The role of molecular mechanism of Ten-Eleven Translocation2 (TET2) family proteins in pathogenesis of cardiovascular diseases (CVDs).Molecular biology reports · 2020Review
- Oxidised Low-Density Lipoprotein and Its Receptor-Mediated Endothelial Dysfunction Are Associated with Coronary Artery Lesions in Kawasaki Disease.Journal of cardiovascular translational research · 2020Article
- LOX-1, the Common Therapeutic Target in Hypercholesterolemia: A New Perspective of Antiatherosclerotic Action of Aegeline.Oxidative medicine and cellular longevity · 2019Article
- Obesity and type-2 diabetes as inducers of premature cellular senescence and ageing.Biogerontology · 2018Review
- AGEs Decreased SIRT3 Expression and SIRT3 Activation Protected AGEs-Induced EPCs' Dysfunction and Strengthened Anti-oxidant Capacity.Inflammation · 2017Article
- Asymmetric Dimethylarginine Induced Apoptosis and Dysfunction of Endothelial Progenitor Cells: Role of Endoplasmic Reticulum Stress Pathway.BioMed research international · 2017Article
- Cinnamaldehyde and allopurinol reduce fructose-induced cardiac inflammation and fibrosis by attenuating CD36-mediated TLR4/6-IRAK4/1 signaling to suppress NLRP3 inflammasome activation.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dyslipidemia increases the risks for atherosclerosis in part by impairing endothelial integrity. Endothelial progenitor cells (EPCs) are thought to contribute to endothelial recovery after arterial injury. Oxidized low-density lipoprotein (ox-LDL) can induce EPC dysfunction, but the underlying mechanism is not well understood. Human EPCs were cultured in endothelial growth medium supplemented with VEGF (10 ng/mL) and bFGF (10 ng/mL). The cells were treated with ox-LDL (50 µg/mL). EPC proliferation was assayed by using CCK8 kits. Expression and translocation of nuclear factor-kabba B (NF-κB) were evaluated. The level of reactive oxygen species (ROS) in cells was measured using H2DCF-DA as a fluorescence probe. The activity of NADPH oxidase activity was determined by colorimetric assay. Ox-LDL significantly decreased the proliferation, migration, and adhesion capacity of EPCs, while significantly increased ROS production and NADPH oxidase expression. Ox-LDL induced NF-κB P65 mRNA expression and translocation in EPCs. Thus ox-LDL can induce EPC dysfunction at least by increasing expression and translocation of NF-κB P65 and NADPH oxidase activity, which represents a new mechanism of lipidemia-induced vascular injury.
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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 OpenQuestion graph.