{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":["Tan JME"],"funding":["NIDDK NIH HHS","NHLBI NIH HHS","NIAMS NIH HHS"],"pubmed_abstract":["Vascular smooth muscle cells (SMCs) normally exist in a contractile state but can undergo fate switching to produce various cell phenotypes in response to pathologic stimuli<sup>1-3</sup>. In atherosclerosis, these phenotypically modulated SMCs regulate plaque composition and influence the risk of major adverse cardiovascular events<sup>4,5</sup>. We found that PRDM16, a transcription factor that is genetically associated with cardiovascular disease, is highly expressed in arterial SMCs and downregulated during SMC fate switching in human and mouse atherosclerosis. Loss of <i>Prdm16</i> in SMCs of mice activates a synthetic modulation program under homeostatic conditions. Single cell analyses show that loss of <i>Prdm16</i> drives a synthetic program in all SMC populations. Upon exposure t"],"journal":["bioRxiv : the preprint server for biology"],"pagination":["2025.02.19.639186"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11870537"],"repository":["biostudies-literature"],"pubmed_title":["PRDM16 controls smooth muscle cell fate in atherosclerosis."],"pmcid":["PMC11870537"],"funding_grant_id":["R01 HL169766","R01 HL148239","R21 AR078650","R01 HL164577","R01 DK120982","R01 DK123356","R01 HL166916","R01 HL150359"],"pubmed_authors":["Miller CL","Lutgens E","Barbara E","Weller AH","Xue C","Reilly MP","Calhoun RP","Tan JME","Seale P","Auguste G","Lim HW","Winter H","Drareni K","Fong S","Cheng L","Maegdefessel L"],"additional_accession":[]},"is_claimable":false,"name":"PRDM16 controls smooth muscle cell fate in atherosclerosis.","description":"Vascular smooth muscle cells (SMCs) normally exist in a contractile state but can undergo fate switching to produce various cell phenotypes in response to pathologic stimuli<sup>1-3</sup>. In atherosclerosis, these phenotypically modulated SMCs regulate plaque composition and influence the risk of major adverse cardiovascular events<sup>4,5</sup>. We found that PRDM16, a transcription factor that is genetically associated with cardiovascular disease, is highly expressed in arterial SMCs and downregulated during SMC fate switching in human and mouse atherosclerosis. Loss of <i>Prdm16</i> in SMCs of mice activates a synthetic modulation program under homeostatic conditions. Single cell analyses show that loss of <i>Prdm16</i> drives a synthetic program in all SMC populations. Upon exposure t","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Feb","modification":"2026-04-18T03:18:22.13Z","creation":"2025-04-04T00:29:43.647Z"},"accession":"S-EPMC11870537","cross_references":{"pubmed":["40027729"],"doi":["10.1101/2025.02.19.639186"]}}