ArticleBritish journal of pharmacology2009
Rosiglitazone via upregulation of Akt/eNOS pathways attenuates dysfunction of endothelial progenitor cells, induced by advanced glycation end products.
Article in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 109 citations in OpenAlex.
- Advanced glycation end products and reactive oxygen species: uncovering the potential role of ferroptosis in diabetic complications.Molecular medicine (Cambridge, Mass.) · 2024Review
- Tuberculosis-diabetes comorbidities: Mechanistic insights for clinical considerations and treatment challenges.World journal of diabetes · 2024Review
- Combined therapeutic strategy based on blocking the deleterious effects of AGEs for accelerating diabetic wound healing.Regenerative biomaterials · 2024Article
- Endothelial progenitor cells as biomarkers of diabetes-related cardiovascular complications.Stem cell research & therapy · 2023Review
- The Disorders of Endometrial Receptivity in PCOS and Its Mechanisms.Reproductive sciences (Thousand Oaks, Calif.) · 2022Review
- Evaluating the role of type 2 diabetes mellitus in rotator cuff tendinopathy: Development and analysis of a novel rat model.Frontiers in endocrinology · 2022Article
- Hax-1 Regulates Radiation-Induced Mitochondrial-Dependent Apoptosis of Uveal Melanoma Cells through PI3K/AKT/eNOS Pathway.Journal of oncology · 2022Article
- Advanced glycation end productions and tendon stem/progenitor cells in pathogenesis of diabetic tendinopathy.World journal of stem cells · 2021Review
- Advanced Glycation End Products Impair Cardiac Atrial Appendage Stem Cells Properties.Journal of clinical medicine · 2021Article
- Therapy for Pulmonary Arterial Hypertension: Glance on Nitric Oxide Pathway.Frontiers in pharmacology · 2021Review
- Uremic Toxins and Vascular Dysfunction.Toxins · 2020Review
- The Impact of Advanced Glycation End-Products (AGEs) on Proliferation and Apoptosis of Primary Stem Cells: A Systematic Review.Stem cells international · 2020Review
- Endothelial Dysfunction in Diabetic Retinopathy.Frontiers in endocrinology · 2020Review
- Rosiglitazone accelerates wound healing by improving endothelial precursor cell function and angiogenesis inPeerJ · 2019Article
- Haem oxygenase-1 up-regulation by rosiglitazone via ROS-dependent Nrf2-antioxidant response elements axis or PPARγ attenuates LPS-mediated lung inflammation.British journal of pharmacology · 2018Article
- Reduced Vitamin D Receptor on Circulating Endothelial Progenitor Cells: A New Risk Factor of Coronary Artery Diseases.Journal of atherosclerosis and thrombosis · 2018Article
- Resveratrol protects late endothelial progenitor cells from TNF-α-induced inflammatory damage by upregulating Krüppel-like factor-2.Molecular medicine reports · 2018Article
- Cigarette Smoke Extract Changes Expression of Endothelial Nitric Oxide Synthase (eNOS) and p16(INK4a) and is Related to Endothelial Progenitor Cell Dysfunction.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
- Preventive effect of rosiglitazone on liver injury in a mouse model of decompression sickness.Diving and hyperbaric medicine · 2017Article
- Regulatory landscape of AGE-RAGE-oxidative stress axis and its modulation by PPARγ activation in high fructose diet-induced metabolic syndrome.Nutrition & metabolism · 2017Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeAdvanced glycation end products (AGEs) and endothelial progenitor cells (EPCs) play key roles in pathogenesis of diabetes-related vascular complications. AGEs can induce dysfunction in EPCs. The peroxisome proliferator-activated receptor-gamma (PPARgamma) agonists are widely used in the treatment of type 2 diabetes, and it remains unknown if they could attenuate EPC dysfunction induced by AGEs. EXPERIMENTAL APPROACH: EPCs isolated from healthy adults were cultured with various concentrations of AGEs (0, 50, 100 and 200 mg L(-1)) with or without rosiglitazone (10 nM), antibody for the receptors for AGE-human serum albumin (anti-receptor for advanced glycation end products (RAGE); 50 microg mL(-1)), phosphatidylinositol-3-kinase (PI3K) inhibitor (LY294002, 5 microM), nitric oxide (NO) synthase inhibitor (L-N(G)-nitro-arginine methyl ester (L-NAME), 100 microM) or sodium nitroprusside (SNP, 25 microM). Proliferation, apoptosis, cell adhesion, migration and NO production in EPCs were assessed, and expressions of endothelial NO synthase (eNOS) and Akt were determined. KEY
resultsNumber, proliferation/migration capacities, eNOS and Akt phosphorylation as well as NO synthesized by EPCs were increased by rosiglitazone and reduced by AGEs. AGEs promoted while rosiglitazone reduced EPC apoptosis. The AGE-induced effects were significantly ameliorated by pre-incubation with rosiglitazone, RAGE antibody and SNP. The beneficial effects of rosiglitazone could be blocked by pretreatment with L-NAME and LY294002. CONCLUSIONS AND IMPLICATIONS: The PPARgamma agonist rosiglitazone increased EPC function and attenuated EPC dysfunction induced by AGEs via upregulating the Akt-eNOS signal pathways of EPCs.
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