{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Li J"],"funding":["NIDA NIH HHS","NCI NIH HHS"],"pagination":["839-853"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8608030"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["41(2)"],"pubmed_abstract":["<h4>Objective</h4>Electronic cigarette (e-cig) use has recently been implicated in promoting atherosclerosis. In this study, we aimed to investigate the mechanism of e-cig exposure accelerated atherosclerotic lesion development. Approach and Results: Eight-week-old ApoE<sup>-/-</sup> mice fed normal laboratory diet were exposed to e-cig vapor (ECV) for 2 hours/day, 5 days/week for 16 weeks. We found that ECV exposure significantly induced atherosclerotic lesions as examined by Oil Red O staining and greatly upregulated TLR9 (toll-like receptor 9) expression in classical monocytes and in the atherosclerotic plaques, which the latter was corroborated by enhanced TLR9 expression in human femoral artery atherosclerotic plaques from e-cig smokers. Intriguingly, we found a significant increase o"],"journal":["Arteriosclerosis, thrombosis, and vascular biology"],"pubmed_title":["Electronic Cigarettes Induce Mitochondrial DNA Damage and Trigger TLR9 (Toll-Like Receptor 9)-Mediated Atherosclerosis."],"pmcid":["PMC8608030"],"funding_grant_id":["P30 DA013429","P01 CA165980","P30 CA072720","R01 DA040619"],"pubmed_authors":["Li J","Steinberg MB","Huang J","Pham K","Cornwell WD","Zhang L","Wang H","Tang MS","Kosmider B","Huynh L","Simborio H","Liu C","Rogers TJ","Zhao H","Thu Thi Le L"],"additional_accession":[]},"is_claimable":false,"name":"Electronic Cigarettes Induce Mitochondrial DNA Damage and Trigger TLR9 (Toll-Like Receptor 9)-Mediated Atherosclerosis.","description":"<h4>Objective</h4>Electronic cigarette (e-cig) use has recently been implicated in promoting atherosclerosis. In this study, we aimed to investigate the mechanism of e-cig exposure accelerated atherosclerotic lesion development. Approach and Results: Eight-week-old ApoE<sup>-/-</sup> mice fed normal laboratory diet were exposed to e-cig vapor (ECV) for 2 hours/day, 5 days/week for 16 weeks. We found that ECV exposure significantly induced atherosclerotic lesions as examined by Oil Red O staining and greatly upregulated TLR9 (toll-like receptor 9) expression in classical monocytes and in the atherosclerotic plaques, which the latter was corroborated by enhanced TLR9 expression in human femoral artery atherosclerotic plaques from e-cig smokers. Intriguingly, we found a significant increase o","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Feb","modification":"2026-05-08T18:00:10.507Z","creation":"2022-02-11T15:50:29.343Z"},"accession":"S-EPMC8608030","cross_references":{"pubmed":["33380174"],"doi":["10.1161/atvbaha.120.315556","10.1161/ATVBAHA.120.315556"]}}