ArticleThe Journal of thoracic and cardiovascular surgery2024
Endothelial to mesenchymal transition in the interleukin-1 pathway during aortic aneurysm formation.
Article in The Journal of thoracic and cardiovascular surgery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 10 citations in OpenAlex.
- SNAI2/SLUG: a key regulator of endothelial-to-mesenchymal transition and vascular remodeling in cardiovascular diseases.Journal of cardiothoracic surgery · 2026Review
- Review
- EndMT in vascular cognitive impairment and dementia: mechanisms, evidence gaps, and therapeutic opportunities.Molecular medicine (Cambridge, Mass.) · 2026Review
- The Potential Role of Endothelial Cells in the Pathophysiology, Diagnosis, and Management of Acute Kawasaki Disease.CJC open · 2026Review
- Response to Shen et al to rapid communication "Fact or fiction: Exploring resident mesenchymal stem cells in abdominal aortic aneurysm from multiple perspectives".Genes & diseases · 2026Article
- Targeting IL-1β: a potential strategy for alleviating the immunopathology of aortic aneurysms.Frontiers in immunology · 2026Review
- Pathological mechanisms and clinical research progress of endothelial dysfunction.Frontiers in cardiovascular medicine · 2026Review
- Therapeutic Strategies for Abdominal Aortic Aneurysm: A Comprehensive Systematic Review.Journal of cardiovascular development and disease · 2025Review
- Single-cell RNA sequencing reveals endothelial cell heterogeneity and Sox18-mediated EndMT in abdominal aortic aneurysm.Theranostics · 2025Article
- Olfactory Receptors and Aortic Aneurysm: Review of Disease Pathways.Journal of clinical medicine · 2024Review
- Endothelial Dysfunction: Molecular Mechanisms and Therapeutic Strategies in Kawasaki Disease.International journal of molecular sciences · 2024Review
- Transcriptomic Analysis of Tight Junction Proteins Demonstrates the Aberrant Expression and Function of Zona Occludens 2 (ZO-2) Protein in Stanford Type A Aortic Dissection.Journal of personalized medicine · 2023Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
objectiveEndothelial to mesenchymal transition may represent a key link between inflammatory stress and endothelial dysfunction seen in aortic aneurysm disease. Endothelial to mesenchymal transition is regulated by interleukin-1β, and previous work has demonstrated an essential role of interleukin-1 signaling in experimental aortic aneurysm models. We hypothesize that endothelial to mesenchymal transition is present in murine aortic aneurysms, and loss of interleukin-1 signaling attenuates this process.
methodsMurine aortic aneurysms were created in novel CDH5-Cre lineage tracking mice by treating the intact aorta with peri-adventitial elastase. Endothelial to mesenchymal transition transcription factors as well as endothelial and mesenchymal cell markers were analyzed via immunohistochemistry and immunofluorescence (n = 10/group). To determine the role of interleukin-1 signaling, endothelial-specific interleukin-1 receptor 1 knockout and wild-type mice (n = 10/group) were treated with elastase. Additionally, C57/BL6 mice were treated with the interleukin-1 receptor 1 antagonist Anakinra (n = 7) or vehicle (n = 8).
resultsElastase treatment yielded greater aortic dilation compared with controls (elastase 97.0% ± 34.0%; control 5.3% ± 4.8%; P < .001). Genetic deletion of interleukin-1 receptor 1 attenuated aortic dilation (control 126.7% ± 38.7%; interleukin-1 receptor 1 knockout 35.2% ± 14.7%; P < .001), as did pharmacologic inhibition of interleukin-1 receptor 1 with Anakinra (vehicle 146.3% ± 30.1%; Anakinra 63.5% ± 23.3%; P < .001). Elastase treatment resulted in upregulation of endothelial to mesenchymal transition transcription factors (Snail, Slug, Twist, ZNF) and mesenchymal cell markers (S100, alpha smooth muscle actin) and loss of endothelial cell markers (vascular endothelial cadherin, endothelial nitric oxide synthase, von Willebrand factor). These changes were attenuated by interleukin-1 receptor 1 knockout and Anakinra treatment.
conclusionsEndothelial to mesenchymal transition occurs in aortic aneurysm disease and is attenuated by loss of interleukin-1 signaling. Endothelial dysfunction through endothelial to mesenchymal transition represents a new and novel pathway in understanding aortic aneurysm disease and may be a potential target for future treatment.
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