{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Garrido AM"],"funding":["British Heart Foundation","National Institute for Health Research (NIHR)","BHF Centre for Research Excellence","BHF Oxbridge Centre for Regenerative Medicine, and the National Institute of Health Research Cambridge Biomedical Research Centre"],"pagination":["1713-1727"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9215197"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["118(7)"],"pubmed_abstract":["Aims
Traditional markers of cell senescence including p16, Lamin B1, and senescence-associated beta galactosidase (SAβG) suggest very high frequencies of senescent cells in atherosclerosis, while their removal via 'senolysis' has been reported to reduce atherogenesis. However, selective killing of a variety of different cell types can exacerbate atherosclerosis. We therefore examined the specificity of senescence markers in vascular smooth muscle cells (VSMCs) and the effects of genetic or pharmacological senolysis in atherosclerosis.Methods and results
We examined traditional senescence markers in human and mouse VSMCs in vitro, and in mouse atherosclerosis. p16 and SAβG increased and Lamin B1 decreased in replicative senescence and stress-induced premature senescence (SIP"],"journal":["Cardiovascular research"],"pubmed_title":["Efficacy and limitations of senolysis in atherosclerosis."],"pmcid":["PMC9215197"],"funding_grant_id":["CH/2000003/12800","PG/13/25/30014","NIHR202375","RG/08/009/25841","RE/18/1/34212","RG/13/14/30314","grants (RG71070, RG84554)","RG/20/2/34763","PG/16/11/32021","PG/16/63/32307","RG84554","PG/14/69/31032","PG/16/24/32090","RG71070"],"pubmed_authors":["Oc S","Foote K","Finigan A","Kaistha A","Shah A","Jorgensen H","Uryga AK","Figg N","Garrido AM","Dobnikar L","Bennett M"],"additional_accession":[]},"is_claimable":false,"name":"Efficacy and limitations of senolysis in atherosclerosis.","description":"Aims
Traditional markers of cell senescence including p16, Lamin B1, and senescence-associated beta galactosidase (SAβG) suggest very high frequencies of senescent cells in atherosclerosis, while their removal via 'senolysis' has been reported to reduce atherogenesis. However, selective killing of a variety of different cell types can exacerbate atherosclerosis. We therefore examined the specificity of senescence markers in vascular smooth muscle cells (VSMCs) and the effects of genetic or pharmacological senolysis in atherosclerosis.Methods and results
We examined traditional senescence markers in human and mouse VSMCs in vitro, and in mouse atherosclerosis. p16 and SAβG increased and Lamin B1 decreased in replicative senescence and stress-induced premature senescence (SIP","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jun","modification":"2026-05-28T07:12:22.545Z","creation":"2024-11-09T07:11:57.964Z"},"accession":"S-EPMC9215197","cross_references":{"pubmed":["34142149"],"doi":["10.1093/cvr/cvab208"]}}