ArticleArquivos brasileiros de cardiologia2020
Atorvastatin Reduces Accumulation of Vascular Smooth Muscle Cells to Inhibit Intimal Hyperplasia via p38 MAPK Pathway Inhibition in a Rat Model of Vein Graft.
Article in Arquivos brasileiros de cardiologia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 10 citations in OpenAlex.
- Atorvastatin Exerts Context-Dependent Metabolic and Beneficial Effects on Behavior and Apoptotic Signaling in a Cafeteria Diet-Induced Metabolic Dysfunction Model.Neurochemical research · 2026Article
- Corilagin inhibits the proliferation of vascular smooth muscle and excessive matrix deposition following vascular injury via the MAPK pathway.Journal of muscle research and cell motility · 2025Article
- The possible modulatory impact of high-dose statin therapy on carotid intima-media thickness: a preliminary study.Postepy w kardiologii interwencyjnej = Advances in interventional cardiology · 2024Article
- Effect of hepatocyte growth factor on mice with hypoxic pulmonary arterial hypertension: a preliminary study.Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2022Article
- Can We Pretreat Vein Grafts with Adiponectin to Improve Their Patency?Arquivos brasileiros de cardiologia · 2021Article
- Anti-Inflammatory Effects of Atorvastatin Therapy in Metabolic Syndrome.Arquivos brasileiros de cardiologia · 2021Article
- Influence of Atorvastatin on Intimal Hyperplasia in the Experimental Model.Arquivos brasileiros de cardiologia · 2020Article
- Pentoxifylline Prevents Restenosis by Inhibiting Cell Proliferation via p38MAPK Pathway in Rat Vein Graft Model.Cell transplantationArticle
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6 authors at 1 institution in 1 country.
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Abstract
backgroundThe rate of saphenous vein graft failure one year after coronary artery bypass grafting ranges from 10% to 25%. The aim of this study was to explore whether atorvastatin can reduce accumulation of vascular smooth muscle cells to inhibit intimal hyperplasia via p38 MAPK pathway inhibition.
methodsForty-five Sprague-Dawley rats were randomized to three groups. Thirty rats received a vein graft operation, and they were randomized to be treated with vehicle or atorvastatin; fifteen rats received a sham operation. We detected intimal hyperplasia by hematoxylin-eosin staining and related protein expression by immunohistochemical and Western blot analysis. Comparisons were analyzed by single-factor analysis of variance and Fisher's least significant difference test, with p < 0.05 considered significant.
resultsThe intima analyzed by hematoxylin-eosin staining was dramatically thicker in the control group than in the atorvastatin group and sham group (p < 0.01). The outcomes of immunohistochemical staining of α-SMA demonstrated that the percentage of α-SMA-positive cells in the control group was higher than in the atorvastatin group (p < 0.01). We also evaluated α-SMA, PCNA, p38 MAPK, and phosphorylation of p38 MAPK after statin treatment by Western blot analysis, and the results indicated that atorvastatin did not lead to p38 MAPK reduction (p < 0.05); it did, however, result in inhibition of p38 MAPK phosphorylation (p < 0.01), and it significantly reduced α-SMA and PCNA levels, in comparison with the control group (p < 0.01).
conclusionWe have demonstrated that atorvastatin can inhibit accumulation of vascular smooth muscle cells by inhibiting the p38 MAPK pathway, and it is capable of inhibiting intimal hyperplasia in a rat vein graft model.
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