ArticleCirculation research2025
Novel Aortic Dissection Model Links Endothelial Dysfunction and Immune Infiltration.
Article in Circulation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- M1 macrophage-derived exosomal miR-155-5p exacerbates aortic dissection via SMAD5-Mediated regulation of vascular smooth muscle cell phenotype.Bioactive materials · 2026Article
- The Potential Role of the Gut-Vascular Axis in Ciprofloxacin-Associated Aggravation of Aortic Dissection.Cardiovascular toxicology · 2026Article
- The aorta in Marfan syndrome: from molecular mechanisms to mechanobiological dysfunction.Cardiovascular research · 2026Review
- Article
- Integrated Single-Cell and Spatial Analysis Reveals a Metabolic-Immune Axis Driving Aortic Dissection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mechanotransduction in Marfan Syndrome and Related Aortic Disorders: Insights from Transcriptomic Analyses.Genes · 2026Review
- Steroid hormone antagonism affords vascular protection in a mouse model of vascular Ehlers-Danlos syndrome.JCI insight · 2026Article
- Endothelial progenitor cells are associated with improved vascular repair in experimental aortic dissection.Scientific reports · 2026Article
- Structural and Signaling Mechanisms of Aortic Wall Failure in Heritable Thoracic Aortic Disease.Cells · 2026Review
- Erosion or Explosion: Integrated Single-Cell Transcriptomics Reveals Cellular Heterogeneity in Aortic Aneurysm and Dissection.Inflammation · 2026Article
- Systematic Disruption of Zebrafish Fibrillin Genes Identifies a Translational Zebrafish Model for Marfan Syndrome.JACC. Basic to translational science · 2026Article
- Structural and transcriptomic alterations underlying the progression of aortic dissection in Fbn1Scientific reports · 2026Article
- Cold exposure increases aortic dissection risk through extracellular cold inducible RNA binding protein and toll like receptor 4 signaling.Scientific reports · 2026Article
- Study on the Role and Mechanism ofJournal of cardiovascular development and disease · 2026Article
- Revealing FPR1 as a potential pathogenic biomarker for aortic dissection based on Mendelian randomization, single-cell transcriptome and clinical data analysis.Biology direct · 2026Article
- Aortic dissection as a disease of vascular wall homeostasis: integrating vasa vasorum-inflammation-metabolism axis for mechanistic insight and clinical translation.Frontiers in immunology · 2026Review
- Type B Aortic Dissection Following Abdominal Aortic Aneurysm Repair in Loeys-Dietz Syndrome: A NovelHuman mutation · 2026Article
- The role of macrophages in aortic physiology and pathophysiology.Frontiers in immunology · 2026Review
- The innate immune axis drives aortic dissection pathogenesis through inflammation and presents novel therapeutic targets.Frontiers in immunology · 2025Review
- Transforming growth factor-beta (TGF-β) in the pathogenesis of hereditary thoracic aneurysm disorders.Cardiovascular pathology : the official journal of the Society for Cardiovascular PathologyReview
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18 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAortic dissection (AD) is the separation of medial layers of the aorta and is a major cause of death in patients with connective tissue disorders such as Marfan syndrome. However, molecular triggers instigating AD, its temporospatial progression, and how vascular cells in each vessel layer interact and participate in the pathological process remain incompletely understood. To unravel the underlying molecular mechanisms of AD, we generated a spontaneous AD mouse model.
methodsWe incorporated a novel missense variant (p.G234D) in
resultsFifty percent of the
conclusionsWe show that interactions involving endothelial cells and macrophages/monocytes in the intima, where the extracellular matrix (ECM) microenvironment contains reduced TGFβ signaling, contribute to the initiation of AD. Our novel AD mouse model provides a unique opportunity to identify target molecules involved in the intimomedial tears that can be utilized for the development of therapeutic strategies.
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