ArticlePloS one2017
Imatinib attenuates cardiac fibrosis by inhibiting platelet-derived growth factor receptors activation in isoproterenol induced model.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- Cardiovascular toxicity induced by immune checkpoint inhibitors: mechanisms linking immune dysregulation and myocardial fibrosis.American journal of clinical and experimental immunology · 2026Review
- Plasmapheresis as a Potential Generalizable Therapy for Myocardial Infarction.Rejuvenation research · 2025Review
- NO/NOS system dysregulation as a key molecular mechanism in chemotherapy-induced cardiotoxicity: a review.Frontiers in cardiovascular medicine · 2025Review
- Effect of high glucose on the gene expression profiling in cardiac fibroblasts from rats at different ages.PeerJ · 2025Article
- Uvaol attenuates TGF-β1-induced epithelial-mesenchymal transition in human alveolar epithelial cells by modulating expression and membrane localization of β-catenin.Frontiers in pharmacology · 2024Article
- Fibroblast activation in response to TGFβ1 is modulated by co-culture with endothelial cells in a vascular organ-on-chip platform.Frontiers in molecular biosciences · 2023Article
- Cardiac Mesenchymal Stem Cells Promote Fibrosis and Remodeling in Heart Failure: Role of PDGF Signaling.JACC. Basic to translational science · 2022Article
- The Pathogenesis of Cardiac Fibrosis: A Review of Recent Progress.International journal of molecular sciences · 2022Review
- Oral Administration ofCirculation reports · 2022Article
- Society for Cardiovascular Magnetic Resonance 2020 Case of the Week series.Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance · 2021Review
- Non-ischemic dilated cardiomyopathy and cardiac fibrosis.Heart failure reviews · 2021Review
- FTZ Ameliorates Diabetic Cardiomyopathy by Inhibiting Inflammation and Cardiac Fibrosis in the Streptozotocin-Induced Model.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Boosting Akt Pathway by Rupatadine Modulates Th17/Tregs Balance for Attenuation of Isoproterenol-Induced Heart Failure in Rats.Frontiers in pharmacology · 2021Article
- Induction of autophagy has protective roles in imatinib-induced cardiotoxicity.Toxicology reports · 2021Article
- M2b macrophages protect against myocardial remodeling after ischemia/reperfusion injury by regulating kinase activation of platelet-derived growth factor receptor of cardiac fibroblast.Annals of translational medicine · 2020Article
- DACT2 regulates structural and electrical atrial remodeling in atrial fibrillation.Journal of thoracic disease · 2020Article
- TBX5 R264K acts as a modifier to develop dilated cardiomyopathy in mice independently of T-box pathway.PloS one · 2020Article
- Macromolecular Crowding as a Tool to Screen Anti-fibrotic Drugs: The Scar-in-a-Jar System Revisited.Frontiers in medicine · 2020Article
- Platelet-derived growth factor receptor-α is essential for cardiac fibroblast survival.American journal of physiology. Heart and circulatory physiology · 2019Article
- Angiogenic Endothelial Cell Signaling in Cardiac Hypertrophy and Heart Failure.Frontiers in cardiovascular medicine · 2019Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac fibrosis is a significant global health problem with limited treatment choices. Although previous studies have shown that imatinib (IMA) inhibited cardiac fibrosis, the anti-fibrotic mechanisms have not been clearly uncovered. The aim of this study is to evaluate whether IMA attenuates cardiac fibrosis by inhibiting platelet-derived growth factor receptors (PDGFR) on isoproterenol (ISO)-induced mice. Adult male C57BL/6 mice were treated with vehicle or ISO ± IMA for one week. After echocardiography examination, the hearts of mice were used for histopathologic, RT-qPCR, and western blot analyses. We found that the ventricular wall thickness, cardiac hypertrophy, and apoptosis were enhanced following ISO treatment. IMA decreased the left ventricular wall thickness, prevented hypertrophy, and inhibited apoptosis induced by ISO. In addition, IMA attenuated the accumulation of collagens and α-smooth muscle actin (α-SMA) (the markers of fibrosis) caused by ISO treatment. Moreover, the expression of fibrosis related genes, and the phosphorylation of PDGFRs in ISO-treated mice hearts were inhibited by IMA as well. However, IMA did not change the expression of the matrix metalloproteinase-9 (MMP-9) in ISO-treated hearts. Furthermore, IMA reduced the expressions of collagens as well as α-SMA caused by activation of PDGFRα in cardiac fibroblasts. Taken together, our data demonstrate that IMA attenuated the cardiac fibrosis by blocking the phosphorylation of PDGFRs in the ISO-induced mice model. This study indicates that IMA could be a potentially therapeutic option for cardiac fibrosis in clinical application.
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