ArticleBritish journal of pharmacology2013
Bleomycin induces endothelial mesenchymal transition through activation of mTOR pathway: a possible mechanism contributing to the sclerotherapy of venous malformations.
Article in British journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.
- Effectiveness of Transarterial Embolization in Treatment of Symptomatic Hepatic Hemangiomas: Systematic Review and Meta-analysis.Cardiovascular and interventional radiology · 2021Pooled it
- Transarterial embolization with bleomycin-lipiodol for symptomatic multifocal hepatic hemangiomas: Concurrent nontarget lesion devascularization via permitted reflux.Radiology case reports · 2026Article
- SNAI2/SLUG: a key regulator of endothelial-to-mesenchymal transition and vascular remodeling in cardiovascular diseases.Journal of cardiothoracic surgery · 2026Review
- Bleomycin ElectroScleroTherapy (BEST): mechanistic parallels to electrochemotherapy, experimental models, and unresolved questions.Radiology and oncology · 2026Review
- Bleomycin sclerotherapy for venous vascular malformations of the tongue.Journal of neurointerventional surgery · 2025Article
- The Role of Bleomycin Sclerotherapy in Venous Malformation Management: A Narrative Review.Life (Basel, Switzerland) · 2025Review
- Recent Advances in Interventional Management of Extracranial Vascular Malformations in Children.Seminars in interventional radiology · 2025Review
- Molecular mechanisms of endothelial-mesenchymal transition and its pathophysiological feature in cerebrovascular disease.Cell & bioscience · 2025Review
- Efficacy of embolo/sclerotherapy in the treatment of high-output cardiac failure caused by peripheral arteriovenous malformations.Frontiers in cardiovascular medicine · 2025Article
- Qimai Feiluoping Decoction Inhibits EndMT to Alleviate Pulmonary Fibrosis by Reducing PI3K/AKT/mTOR Pathway-Mediated the Restoration of Autophagy.Journal of inflammation research · 2025Article
- Endothelial Foxo1 Phosphorylation Inhibition via Aptamer-Liposome Alleviates OPN-Induced Pathological Vascular Remodeling Following Spinal Cord Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Lymphatic Malformations: Review of Diagnosis and Management for the Interventional Radiologist.Seminars in interventional radiology · 2024Review
- Elucidating the crosstalk between endothelial-to-mesenchymal transition (EndoMT) and endothelial autophagy in the pathogenesis of atherosclerosis.Vascular pharmacology · 2024Review
- Comparison of bleomycin polidocanol foam vs electrochemotherapy combined with polidocanol foam for treatment of venous malformations.Journal of vascular surgery. Venous and lymphatic disorders · 2024Article
- Clinical outcomes and predictors of bleomycin polidocanol foam sclerotherapy treatment response in venous malformations.The Journal of international medical research · 2024Article
- A technical review of percutaneous sclerotherapy with bleomycin for giant hepatic venous malformation.CVIR endovascular · 2023Article
- Venous Malformations.Seminars in interventional radiology · 2022Review
- Linagliptin ameliorates pulmonary fibrosis in systemic sclerosis mouse model via inhibition of endothelial-to-mesenchymal transition.Molecular and cellular biochemistry · 2022Article
- Slight up-regulation of Kir2.1 channel promotes endothelial progenitor cells to transdifferentiate into a pericyte phenotype by Akt/mTOR/Snail pathway.Journal of cellular and molecular medicine · 2021Article
- Endothelial-to-mesenchymal transition in systemic sclerosis.Clinical and experimental immunology · 2021Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeBleomycin (BLM), one of the most common sclerosants, is often used to treat venous malformations (VMs). The present study was designed to investigate whether endothelial mesenchymal transition (EndoMT) contributes to the therapeutic effects of BLM. EXPERIMENTAL APPROACH: Endothelial and mesenchymal markers of HUVECs were measured by immunofluorescence, real-time quantitative PCR and Western blot analysis. Cell migration and tube formation assays were performed to evaluate endothelial cell function. Slug small-interfering RNA and specific inhibitors [Z-VAD-FMK for pan caspases, rapamycin for mammalian target of rapamycin (mTOR)] were used to investigate the mechanism. KEY
resultsLong term (48 h or longer) treatment with BLM (0.1 mU·mL(-1) ) induced EndoMT in HUVECs, as manifested by a reduction in the expression of vascular endothelial-cadherin and an up-regulation in the expression of α-smooth muscle actin and fibroblast specific protein-1, as well as activation of the transcription factor Slug. The size and protein content of the transformed cells were increased. BLM also enhanced the migration of HUVECs but diminished their tube formation. By employing rapamycin, we demonstrated that activation of the mTOR pathway is involved in BLM-induced EndoMT in HUVECs. CONCLUSIONS AND IMPLICATIONS: Our results show that a Slug-dependent EndoMT process is involved in BLM-induced therapeutic effects on endothelial cells and, more importantly, indicate the potential role of this process in the sclerotherapy of VMs.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.