ArticleArchives of medical sciences. Atherosclerotic diseases2020
Atheroprotective effects of 17β-oestradiol are mediated by peroxisome proliferator-activated receptor γ in human coronary artery smooth muscle cells.
Article in Archives of medical sciences. Atherosclerotic diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- G protein-coupled estrogen receptor GPR30 exerts vasoprotective effects in apolipoprotein E-deficient mice.Archives of medical science : AMS · 2026Article
- Effect of Copper-Containing Stainless Steel on Apoptosis of Coronary Artery Smooth Muscle Cells.Iranian journal of public health · 2021Article
- 17β-Estradiol Promotes Apoptosis of HepG2 Cells Caused by Oxidative Stress by Increasing Foxo3a Phosphorylation.Frontiers in pharmacology · 2021Article
- Toward the Effective Bioengineering of a Pathological Tissue for Cardiovascular Disease Modeling: Old Strategies and New Frontiers for Prevention, Diagnosis, and Therapy.Frontiers in cardiovascular medicine · 2020Review
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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
introduction17β-oestradiol (E2) mediates vasculoprotection in various preclinical and clinical models of atherosclerosis and neointimal hyperplasia. However, the molecular mechanisms underlying these effects are still not fully elucidated. Previous studies have demonstrated the essential role of the peroxisome-proliferator-activated-receptor-γ (PPARγ) in mediating vasculoprotective effects of E2 MATERIAL AND
methodsPrimary HCASMC were stimulated with E2 (10 nM), the selective oestrogen receptor α (ERα) agonist propylpyrazole triol (PPT) (50 nM) and the selective ERα antagonist methyl-piperidino-pyrazole (MPP) (1 µM), respectively. Changes in PPARγ mRNA, protein expression, and DNA binding affinity were assessed.
resultsE2 significantly increased PPARγ expression in HCASMC (1.95 ±0.41-fold;
conclusionsThe present study identifies PPARγ as an important downstream mediator of E2-related atheroprotective effects in HCASMC. PPARγ agonism might be a promising therapeutic strategy to prevent neointimal hyperplasia and consecutive cardiovascular events in postmenopausal women with depleted E2 plasma levels.
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