ArticleClinical and translational medicine2020
Evidence for endothelial-to-mesenchymal transition in human brain arteriovenous malformations.
Article in Clinical and translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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Who cites it
34 citing papers in PubMed, 62 citations in OpenAlex.
- Extracellular matrix remodeling and internal elastic lamina alterations in cerebral arteriovenous malformations: Insights into vascular wall biology.Neurosurgical review · 2026Review
- Human stem cell models in cerebral cavernous malformations.Stem cell research & therapy · 2026Review
- EndMT in vascular cognitive impairment and dementia: mechanisms, evidence gaps, and therapeutic opportunities.Molecular medicine (Cambridge, Mass.) · 2026Review
- Advances in the Genetics and Molecular Biology of Brain Arteriovenous Malformations.Translational stroke research · 2026Review
- Trametinib Decreased Intracerebral Hemorrhages and Endothelial-to-Mesenchymal Transition in KRASStroke · 2026Article
- Endothelial-Mesenchymal transition in cerebrovascular diseases: molecular mechanisms and promising pharmacological strategies.Molecular biology reports · 2026Review
- Endothelial-to-mesenchymal transition in atherosclerosis: mechanisms, therapeutic targets, and future perspectives.Frontiers in cell and developmental biology · 2026Review
- The S1PR1-CCN1 axis drives endothelial-to-mesenchymal transition and vascular instability in brain arteriovenous malformations.European journal of medical research · 2025Article
- Reconceptualizing Endothelial-to-mesenchymal transition in atherosclerosis: Signaling pathways and prospective targeting strategies.Journal of advanced research · 2025Review
- Characterizing the Microenvironment of Cerebral Arteriovenous Malformations to Test Novel Treatment Modalities.Brain sciences · 2025Review
- Tissue-Resident Mesenchymal Stem/stromal Cells (MSC) Modulate the Angiogenic Processes in Brain Arteriovenous Malformations (bAVM).Stem cell reviews and reports · 2025Article
- Molecular mechanisms of endothelial-mesenchymal transition and its pathophysiological feature in cerebrovascular disease.Cell & bioscience · 2025Review
- The role of ATF3 in precision medicine of brain arteriovenous malformation: based on endothelial cell proliferation.Frontiers in immunology · 2025Article
- Basic Knowledge and Overview of Brain AVMs.Journal of neuroendovascular therapy · 2025Review
- Review
- Advances in regulating endothelial-mesenchymal transformation through exosomes.Stem cell research & therapy · 2024Review
- Pathophysiology in Brain Arteriovenous Malformations: Focus on Endothelial Dysfunctions and Endothelial-to-Mesenchymal Transition.Biomedicines · 2024Review
- Gastric Cancer Mesenchymal Stem Cells Trigger Endothelial Cell Functional Changes to Promote Cancer Progression.Stem cell reviews and reports · 2024Article
- Endothelial-to-Mesenchymal Transition in an Hereditary Hemorrhagic Telangiectasia-like Pediatric Case of Multiple Pulmonary Arteriovenous Malformations.International journal of molecular sciences · 2024Article
- High glutamine increases stroke risk by inducing the endothelial-to-mesenchymal transition in moyamoya disease.MedComm · 2024Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBrain arteriovenous malformations (AVMs) are rare, potentially devastating cerebrovascular lesions that can occur in both children and adults. AVMs are largely sporadic and the basic disease biology remains unclear, limiting advances in both detection and treatment. This study aimed to investigate human brain AVMs for endothelial-to-mesenchymal transition (EndMT), a process recently implicated in cerebral cavernous malformations (CCMs).
methodsWe used 29 paraffin-embedded and 13 fresh/frozen human brain AVM samples to profile expression of panels of EndMT-associated proteins and RNAs. CCMs, a cerebrovascular disease also characterized by abnormal vasculature, were used as a primary comparison, given that EndMT specifically contributes to CCM disease biology. AVM-derived cell lines were isolated from three fresh, surgical AVM samples and characterized by protein expression.
resultsWe observed high collagen deposition, high PAI-1 expression, and expression of EndMT-associated transcription factors such as KLF4, SNAI1, and SNAI2 and mesenchymal-associated markers such as VIM, ACTA2, and S100A4. SMAD-dependent TGF-β signaling was not strongly activated in AVMs and this pathway may be only partially involved in mediating EndMT. Using serum-free culture conditions, we isolated myofibroblast-like cell populations from AVMs that expressed a unique range of proteins associated with mature cell types and with EndMT. Conditioned medium from these cells led to increased proliferation of HUVECs and SMCs.
conclusionsCollectively, our results suggest a role for EndMT in AVM disease. This may lead to new avenues for disease models to further our understanding of disease mechanisms, and to the development of improved diagnostics and therapeutics.
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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.