ArticleArteriosclerosis, thrombosis, and vascular biology2013
Loss of CDKN2B promotes p53-dependent smooth muscle cell apoptosis and aneurysm formation.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.
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Who cites it
71 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.
- Dissecting the Genetic Architecture of Intracranial Aneurysms.Circulation. Genomic and precision medicine · 2025Pooled it
- CDKN2B Inhibits Vascular Smooth Muscle Phenotypic Switching in Corpus Spongiosum Surrounding the Urethral Plate in Hypospadias.Biomedicines · 2025Article
- Coronary artery disease-associated variants regulate vascular smooth muscle cell gene expression.Nature cardiovascular research · 2025Article
- Enhancer-targeting CRISPR screens at coronary artery disease loci suggest shared mechanisms of disease risk.medRxiv : the preprint server for health sciences · 2025Article
- The role of longevity-related genetic variant interactions as predictors of survival after 85 years of age.Mechanisms of ageing and development · 2024Article
- Top Five Stories of the Cellular Landscape and Therapies of Atherosclerosis: Current Knowledge and Future Perspectives.Current medical science · 2024Review
- Association of Genetic Polymorphisms with Abdominal Aortic Aneurysm in the Processes of Apoptosis, Inflammation, and Cholesterol Metabolism.Medicina (Kaunas, Lithuania) · 2023Article
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- Role of vascular smooth muscle cell clonality in atherosclerosis.Frontiers in cardiovascular medicine · 2023Review
- The contribution of matrix metalloproteinases and their inhibitors to the development, progression, and rupture of abdominal aortic aneurysms.Frontiers in cardiovascular medicine · 2023Review
- Linking single nucleotide polymorphisms to signaling blueprints in abdominal aortic aneurysms.Scientific reports · 2022Article
- Fibromuscular Dysplasia and Abdominal Aortic Aneurysms Are Dimorphic Sex-Specific Diseases With Shared Complex Genetic Architecture.Circulation. Genomic and precision medicine · 2022Article
- Defective efferocytosis of vascular cells in heart disease.Frontiers in cardiovascular medicine · 2022Review
- Through network pharmacology and molecular docking to explore the underlying mechanism ofFrontiers in physiology · 2022Article
- Advanced Oxidative Protein Products Drive Trophoblast Cells Into Senescence by Inhibiting the Autophagy: The Potential Implication of Preeclampsia.Frontiers in cell and developmental biology · 2022Article
- Efferocytosis in multisystem diseases (Review).Molecular medicine reports · 2022Review
- Vascular Smooth Muscle Cells in Aortic Aneurysm: From Genetics to Mechanisms.Journal of the American Heart Association · 2021Article
- Chitinase 3 like 1 is a regulator of smooth muscle cell physiology and atherosclerotic lesion stability.Cardiovascular research · 2021Article
- Wild-Type and Mutant FUS Expression Reduce Proliferation and Neuronal Differentiation Properties of Neural Stem Progenitor Cells.International journal of molecular sciences · 2021Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
27 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveGenomewide association studies have implicated allelic variation at 9p21.3 in multiple forms of vascular disease, including atherosclerotic coronary heart disease and abdominal aortic aneurysm. As for other genes at 9p21.3, human expression quantitative trait locus studies have associated expression of the tumor suppressor gene CDKN2B with the risk haplotype, but its potential role in vascular pathobiology remains unclear. METHODS AND
resultsHere we used vascular injury models and found that Cdkn2b knockout mice displayed the expected increase in proliferation after injury, but developed reduced neointimal lesions and larger aortic aneurysms. In situ and in vitro studies suggested that these effects were attributable to increased smooth muscle cell apoptosis. Adoptive bone marrow transplant studies confirmed that the observed effects of Cdkn2b were mediated through intrinsic vascular cells and were not dependent on bone marrow-derived inflammatory cells. Mechanistic studies suggested that the observed increase in apoptosis was attributable to a reduction in MDM2 and an increase in p53 signaling, possibly due in part to compensation by other genes at the 9p21.3 locus. Dual inhibition of both Cdkn2b and p53 led to a reversal of the vascular phenotype in each model.
conclusionsThese results suggest that reduced CDKN2B expression and increased smooth muscle cell apoptosis may be one mechanism underlying the 9p21.3 association with aneurysmal disease.
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Registered trials
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.