<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Li J</submitter><funding>NIDA NIH HHS</funding><funding>NCI NIH HHS</funding><pagination>839-853</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8608030</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>41(2)</volume><pubmed_abstract>&lt;h4>Objective&lt;/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&lt;sup>-/-&lt;/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</pubmed_abstract><journal>Arteriosclerosis, thrombosis, and vascular biology</journal><pubmed_title>Electronic Cigarettes Induce Mitochondrial DNA Damage and Trigger TLR9 (Toll-Like Receptor 9)-Mediated Atherosclerosis.</pubmed_title><pmcid>PMC8608030</pmcid><funding_grant_id>P30 DA013429</funding_grant_id><funding_grant_id>P01 CA165980</funding_grant_id><funding_grant_id>P30 CA072720</funding_grant_id><funding_grant_id>R01 DA040619</funding_grant_id><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Steinberg MB</pubmed_authors><pubmed_authors>Huang J</pubmed_authors><pubmed_authors>Pham K</pubmed_authors><pubmed_authors>Cornwell WD</pubmed_authors><pubmed_authors>Zhang L</pubmed_authors><pubmed_authors>Wang H</pubmed_authors><pubmed_authors>Tang MS</pubmed_authors><pubmed_authors>Kosmider B</pubmed_authors><pubmed_authors>Huynh L</pubmed_authors><pubmed_authors>Simborio H</pubmed_authors><pubmed_authors>Liu C</pubmed_authors><pubmed_authors>Rogers TJ</pubmed_authors><pubmed_authors>Zhao H</pubmed_authors><pubmed_authors>Thu Thi Le L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Electronic Cigarettes Induce Mitochondrial DNA Damage and Trigger TLR9 (Toll-Like Receptor 9)-Mediated Atherosclerosis.</name><description>&lt;h4>Objective&lt;/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&lt;sup>-/-&lt;/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</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Feb</publication><modification>2026-05-08T18:00:10.507Z</modification><creation>2022-02-11T15:50:29.343Z</creation></dates><accession>S-EPMC8608030</accession><cross_references><pubmed>33380174</pubmed><doi>10.1161/atvbaha.120.315556</doi><doi>10.1161/ATVBAHA.120.315556</doi></cross_references></HashMap>