| http://purl.uniprot.org/citations/34272458 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/34272458 | http://www.w3.org/2000/01/rdf-schema#comment | "Senescent vascular cells are detected in atherosclerotic lesion, and its involvement in the development of atherosclerosis has been revealed; however, whether and the mechanism by which endothelial cell (EC) senescence is causally implicated in atherosclerosis remains unclear. We here investigate a role of EC senescence in atherosclerosis by utilizing EC-specific progeroid mice that overexpress the dominant negative form of telomeric repeat-binding factor 2 under the control of the Tie2 or vascular endothelial cadherin promoter. EC-specific progeria accelerated atherosclerosis in mice with target deletion of ApoE. Mechanistically, senescent ECs were markedly sensitive for inflammation-mediated VCAM-1 induction, leading to enhanced monocyte adhesion. Inhibition of NF-κB signaling abolished the enhanced inflammatory responses in senescent ECs, while NF-κB nuclear translocation in response to TNF-α were similar between young and senescent ECs. We found a higher association of VCAM-1 gene with active histone H3 trimethylated on lysine 4, leading to increased NF-κB accessibility in senescent ECs. Our data revealed that EC cellular senescence causes endothelial hyper-inflammability through epigenetic alteration, which consequently accelerates atherosclerosis. Therefore, EC senescence is a promising therapeutic target for the prevention and/or treatment of atherosclerotic disease in elderly population."xsd:string |
| http://purl.uniprot.org/citations/34272458 | http://purl.org/dc/terms/identifier | "doi:10.1038/s41598-021-94097-5"xsd:string |
| http://purl.uniprot.org/citations/34272458 | http://purl.uniprot.org/core/author | "Honda S."xsd:string |
| http://purl.uniprot.org/citations/34272458 | http://purl.uniprot.org/core/author | "Ikeda K."xsd:string |
| http://purl.uniprot.org/citations/34272458 | http://purl.uniprot.org/core/author | "Matoba S."xsd:string |
| http://purl.uniprot.org/citations/34272458 | http://purl.uniprot.org/core/author | "Emoto N."xsd:string |
| http://purl.uniprot.org/citations/34272458 | http://purl.uniprot.org/core/author | "Yamazaki E."xsd:string |
| http://purl.uniprot.org/citations/34272458 | http://purl.uniprot.org/core/author | "Urata R."xsd:string |
| http://purl.uniprot.org/citations/34272458 | http://purl.uniprot.org/core/date | "2021"xsd:gYear |
| http://purl.uniprot.org/citations/34272458 | http://purl.uniprot.org/core/name | "Sci Rep"xsd:string |
| http://purl.uniprot.org/citations/34272458 | http://purl.uniprot.org/core/pages | "14608"xsd:string |
| http://purl.uniprot.org/citations/34272458 | http://purl.uniprot.org/core/title | "Cellular senescence promotes endothelial activation through epigenetic alteration, and consequently accelerates atherosclerosis."xsd:string |
| http://purl.uniprot.org/citations/34272458 | http://purl.uniprot.org/core/volume | "11"xsd:string |
| http://purl.uniprot.org/citations/34272458 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/34272458 |
| http://purl.uniprot.org/citations/34272458 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/34272458 |
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