ArticleThe American journal of pathology2008
Potential role of CYLD (Cylindromatosis) as a deubiquitinating enzyme in vascular cells.
Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- Endothelial Cell TRIM47 Triggers Blood-Brain Barrier Disruption via CYLD Ubiquitination Degradation in an Intracerebral Hemorrhage Model.Neuroscience bulletin · 2026Article
- The Role of the PI3K/Akt/mTOR Pathway in Atherosclerosis: Mechanisms, Therapeutic Potential, and Emerging Targeted Treatments.Current atherosclerosis reports · 2025Review
- CYLD links the TRAF6/sNASP axis to TLR4 signaling in sepsis-induced acute lung injury.Cellular and molecular life sciences : CMLS · 2025Article
- A computational approach for structural and functional analyses of disease-associated mutations in the human CYLD gene.Genomics & informatics · 2024Article
- The Potential of Cylindromatosis (CYLD) as a Therapeutic Target in Oxidative Stress-Associated Pathologies: A Comprehensive Evaluation.International journal of molecular sciences · 2023Review
- The Role of Deubiquitinases in Vascular Diseases.Journal of cardiovascular translational research · 2020Review
- The Genetic Dissection ofFrontiers in cardiovascular medicine · 2020Article
- Vitamin E δ-tocotrienol inhibits TNF-α-stimulated NF-κB activation by up-regulation of anti-inflammatory A20 via modulation of sphingolipid including elevation of intracellular dihydroceramides.The Journal of nutritional biochemistry · 2019Article
- USP20 (Ubiquitin-Specific Protease 20) Inhibits TNF (Tumor Necrosis Factor)-Triggered Smooth Muscle Cell Inflammation and Attenuates Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- CYLD Promotes TNF-Mediators of inflammation · 2016Article
- The TRAF-interacting protein (TRAIP) is a novel E2F target with peak expression in mitosis.Oncotarget · 2015Article
- Dysfunction of the ubiquitin-proteasome system in atherosclerotic cardiovascular disease.American journal of cardiovascular disease · 2015Review
- CYLD-mediated signaling and diseases.Current drug targets · 2015Review
- Human coronary heart disease: importance of blood cellular miR-2909 RNomics.Molecular and cellular biochemistry · 2014Article
- A pro-inflammatory role of deubiquitinating enzyme cylindromatosis (CYLD) in vascular smooth muscle cells.Biochemical and biophysical research communications · 2012Article
- Regulation of NF-κB by deubiquitinases.Immunological reviews · 2012Review
- Inflammation, endoplasmic reticulum stress, autophagy, and the monocyte chemoattractant protein-1/CCR2 pathway.Circulation research · 2012Review
- The ubiquitin-proteasome system and cardiovascular disease.Progress in molecular biology and translational science · 2012Review
- Sent to destroy: the ubiquitin proteasome system regulates cell signaling and protein quality control in cardiovascular development and disease.Circulation research · 2010Review
- On to the road to degradation: atherosclerosis and the proteasome.Cardiovascular research · 2010Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Data from several studies suggest that the ubiquitin-proteasome system may play a role in the progression of atherosclerosis. Here, we examined the potential role of the deubiquitinating enzyme CYLD (cylindromatosis), mutation of which has been reported to cause familial cylindromatosis. Northern blot analysis revealed expression of CYLD mRNA in the aorta, as well as in cultured human aortic endothelial cells (ECs) and vascular smooth muscle cells. Treatment with recombinant tumor necrosis factor (TNF)-alpha significantly increased CYLD expression in ECs and vascular smooth muscle cells. Immunostaining showed CYLD expression in atherosclerotic lesions from human carotid arteries and up-regulation of CYLD expression in the neointima of rat carotid arteries after balloon injury. Overexpression of CYLD in ECs resulted in inhibition of TNF-alpha-induced nuclear factor-kappaB activity through deubiquitination of TNFR-associated factor 2 (TRAF2), whereas overexpression of catalytically inactive CYLD had no effect. CYLD overexpression also inhibited expression of cyclin D1 and activation of the E2F pathway through deubiquitination of the upstream molecule Bcl-3 and inhibition of its translocation into the nucleus. Overexpressed CYLD also significantly inhibited cell viability. Furthermore, overexpression of CYLD in rat balloon-injured carotid artery attenuated neointimal formation through inactivation of nuclear factor-kappaB and E2F. In conclusion, these data demonstrate that the deubiquitinating enzyme CYLD may inhibit inflammation and proliferation in vascular cells and may represent a novel target for the treatment or prevention of atherosclerosis.
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