ArticleCJC open2025
Relationship Between Vascular Smooth Muscle Cell Phenotype and Degeneration of Elastin in the Aortic Media in Patients With Acute Aortic Dissection.
Article in CJC open, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- The role of Smoothelin-B in abdominal aortic aneurysm formation.Biochemistry and biophysics reports · 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
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Acute aortic dissection (AAD) is a life-threatening disease with no known detailed pathogenesis in a certain percentage of patients. Although phenotypic modulation of vascular smooth muscle cells (VSMCs) and degeneration of the extracellular matrix (ECM) are known to occur in AAD, the relationship between the VSMC phenotype and ECM degeneration is unclear. We designed this study to identify the relationship between the VSMC phenotype and ECM disorders in dissected aortic media. Methods: The tunica media of the ascending aorta was collected from 24 patients with AAD and 17 control autopsy cases. Immunostaining and immunoblotting were performed using antibodies against the contractile phenotypic markers, smooth muscle myosin heavy chain (SM-MHC) and smoothelin, and the synthetic marker, S100A4. Results: Immunostaining and immunoblotting demonstrated that the expression levels of both SM-MHC and smoothelin were significantly decreased, whereas S100A4 expression levels were elevated, in the tunica media from patients with AAD. The expression level of elastin, a major component of the ECM, was significantly decreased in patients with AAD. There were significant positive correlations between the expression levels of contractile markers, such as SM-MHC, smoothelin, and elastin. Conclusions: Phenotypic modulation of VSMCs and matrix degeneration in the tunica media of patients with AAD may interact and this phenomenon may contribute to the pathogenesis of AAD.
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Registered trials
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