ArticleJournal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban2017
Celastrol protects TGF-β1-induced endothelial-mesenchymal transition.
Article in Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Tumor-targeted Exosomal Delivery of Celastrol for Enhanced Therapeutic Efficacy in NSCLC.Theranostics · 2026Article
- Linc-ROR Modulates the Endothelial-Mesenchymal Transition of Endothelial Progenitor Cells through the miR-145/Smad3 Signaling Pathway.Physiological research · 2024Article
- Hyperoxia exposure promotes endothelial-mesenchymal transition and inhibits regulatory T cell function in human pulmonary microvascular endothelial cells.Frontiers in pediatrics · 2024Article
- Review
- METTL3 Promotes Endothelium-Mesenchymal Transition of Pulmonary Artery Endothelial Cells by Regulating TRPC6/Calcineurin/NFAT Signaling Pathways.Evidence-based complementary and alternative medicine : eCAM · 2023Article
- Celastrol inhibits pathologic neovascularization in oxygen-induced retinopathy by targeting the miR-17-5p/HIF-1α/VEGF pathway.Cell cycle (Georgetown, Tex.) · 2022Article
- Celastrol suppresses nitric oxide synthases and the angiogenesis pathway in colorectal cancer.Free radical research · 2019Article
- The therapeutic potential of targeting the endothelial-to-mesenchymal transition.Angiogenesis · 2019Review
- Emerging role of Twist1 in fibrotic diseases.Journal of cellular and molecular medicine · 2018Review
- Celastrol improves self-renewal and differentiation of human tendon-derived stem cells by suppressing Smad7 through hypoxia.Stem cell research & therapy · 2017Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The endothelial-to-mesenchymal transition (EndMT) in endothelial cells contributes to the development of cardiac fibrosis, ultimately leading to cardiac remodeling. In this study, the effects and molecular mechanisms of celastrol (CEL) on transforming growth factor-β1 (TGF-β1)-induced EndMT in human umbilical vein endothelial (HUVEC-12) cells were investigated. The presented data demonstrated that CEL significantly blocked the morphology change of HUVEC-12 cells induced by TGF-β1 without cell cytotoxicity. In accordance with these findings, CEL blocked TGF-β1-induced EndMT as evidenced by the inhibition of the mesenchymal markers, including collagen I, III, α-SMA, fibronectin mRNA expression, and the increase in the mRNA expression of endothelial cell marker CD31. These changes were also confirmed by double immunofluorescence staining of CD31 and vimentin. The in vitro scratch assay showed that CEL inhibited the migration capacity of the transitioned endothelial cells induced by TGF-β1. Further experiments showed that the beneficial effect of CEL on blocking the EndMT in HUVEC-12 cells was associated with the suppression of the TGF-β1/Smads signalling pathway, which was also confirmed by the inhibition of its downstream transcription factor snail1, twist1, twist2, ZEB1 and ZEB2. These results indicate that CEL blocks TGF-β1-induced EndMT through TGF-β1/Smads signalling pathway and suggest that it may be a feasible therapy for cardiac fibrosis diseases.
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