ArticleJCI insight2023
CCN2 deficiency in smooth muscle cells triggers cell reprogramming and aggravates aneurysm development.
Article in JCI insight, 2023. 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.
- Smooth muscle cell spheroids as 3D model of phenotypic plasticity and matrix deposition revealed by 2D-3D proteomics.Scientific reports · 2026Article
- Protectin D1/GPR37 Signaling Enhances Macrophage-Dependent Efferocytosis to Attenuate Experimental Abdominal Aortic Aneurysm Formation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Extracellular matrix in vascular homeostasis and disease.Nature reviews. Cardiology · 2025Review
- METTL3 obstructs vascular smooth muscle cells osteogenic reprogramming by methylating Runx2 in chronic kidney disease.Communications biology · 2025Article
- Single-Cell Transcriptomics Identifies Selective Lineage-Specific Regulation of Genes in Aortic Smooth Muscle Cells in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Therapeutic Targeting of Signaling Pathways in Abdominal Aortic Aneurysm: From Pathogenesis to Precision Medicine.Drug design, development and therapy · 2025Review
- Hippo in smooth muscle - a therapeutic target in vascular diseases driven by aging and hypertension.Frontiers in physiology · 2025Review
- Cellular communication network factor 2 regulates smooth muscle cell transdifferentiation and lipid accumulation in atherosclerosis.Cardiovascular research · 2024Article
- Affinity-Enriched Plasma Proteomics for Biomarker Discovery in Abdominal Aortic Aneurysms.Proteomes · 2024Article
- Smooth muscle-specific deletion of cellular communication network factor 2 causes severe aorta malformation and atherosclerosis.Cardiovascular research · 2024Article
- Article
- Colchicine Blocks Abdominal Aortic Aneurysm Development by Maintaining Vascular Smooth Muscle Cell Homeostasis.International journal of biological sciences · 2024Article
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Authors and funding
7 authors.
Funding
Abstract
Vascular smooth muscle cell (SMC) phenotypic switching is widely recognized as a key mechanism responsible for the pathogenesis of several aortic diseases, such as aortic aneurysm. Cellular communication network factor 2 (CCN2), often upregulated in human pathologies and animal disease models, exerts myriad context-dependent biological functions. However, current understanding of the role of SMC-CCN2 in SMC phenotypic switching and its function in the pathology of abdominal aortic aneurysm (AAA) is lacking. Here, we show that SMC-restricted CCN2 deficiency causes AAA in the infrarenal aorta of angiotensin II-infused (Ang II-infused) hypercholesterolemic mice at a similar anatomic location to human AAA. Notably, the resistance of naive C57BL/6 WT mice to Ang II-induced AAA formation is lost upon silencing of CCN2 in SMC. Furthermore, the pro-AAA phenotype of SMC-CCN2-KO mice is recapitulated in a different model that involves the application of elastase-β-aminopropionitrile. Mechanistically, our findings reveal that CCN2 intersects with TGF-β signaling and regulates SMC marker expression. Deficiency of CCN2 triggers SMC reprograming associated with alterations in Krüppel-like factor 4 and contractile marker expression, and this reprograming likely contributes to the development of AAA in mice. These results identify SMC-CCN2 as potentially a novel regulator of SMC phenotypic switching and AA biology.
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