<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Kuntic M</submitter><funding>Boehringer Ingelheim Foundation</funding><funding>NHLBI NIH HHS</funding><funding>Foundation Heart of Mainz</funding><funding>University Mainz</funding><pagination>2472-2483</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7340357</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>41(26)</volume><pubmed_abstract>&lt;h4>Aims&lt;/h4>Electronic (e)-cigarettes have been marketed as a 'healthy' alternative to traditional combustible cigarettes and as an effective method of smoking cessation. There are, however, a paucity of data to support these claims. In fact, e-cigarettes are implicated in endothelial dysfunction and oxidative stress in the vasculature and the lungs. The mechanisms underlying these side effects remain unclear. Here, we investigated the effects of e-cigarette vapour on vascular function in smokers and experimental animals to determine the underlying mechanisms.&lt;h4>Methods and results&lt;/h4>Acute e-cigarette smoking produced a marked impairment of endothelial function in chronic smokers determined by flow-mediated dilation. In mice, e-cigarette vapour without nicotine had more detrimental eff</pubmed_abstract><journal>European heart journal</journal><pubmed_title>Short-term e-cigarette vapour exposure causes vascular oxidative stress and dysfunction: evidence for a close connection to brain damage and a key role of the phagocytic NADPH oxidase (NOX-2).</pubmed_title><pmcid>PMC7340357</pmcid><funding_grant_id>R01 HL151626</funding_grant_id><pubmed_authors>Munzel T</pubmed_authors><pubmed_authors>Kroller-Schon S</pubmed_authors><pubmed_authors>Filippou K</pubmed_authors><pubmed_authors>Vujacic-Mirski K</pubmed_authors><pubmed_authors>Bayo Jimenez MT</pubmed_authors><pubmed_authors>Varveri F</pubmed_authors><pubmed_authors>Daiber A</pubmed_authors><pubmed_authors>Daub S</pubmed_authors><pubmed_authors>Gori T</pubmed_authors><pubmed_authors>Hahad O</pubmed_authors><pubmed_authors>Kuntic M</pubmed_authors><pubmed_authors>Schmidt FP</pubmed_authors><pubmed_authors>Stamm P</pubmed_authors><pubmed_authors>Steven S</pubmed_authors><pubmed_authors>Bruckl V</pubmed_authors><pubmed_authors>Kalinovic S</pubmed_authors><pubmed_authors>Keaney JF</pubmed_authors><pubmed_authors>Frenis K</pubmed_authors><pubmed_authors>Kvandova M</pubmed_authors><pubmed_authors>Huesmann R</pubmed_authors><pubmed_authors>Hoffmann T</pubmed_authors><pubmed_authors>Oelze M</pubmed_authors><pubmed_authors>Al Zuabi A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Short-term e-cigarette vapour exposure causes vascular oxidative stress and dysfunction: evidence for a close connection to brain damage and a key role of the phagocytic NADPH oxidase (NOX-2).</name><description>&lt;h4>Aims&lt;/h4>Electronic (e)-cigarettes have been marketed as a 'healthy' alternative to traditional combustible cigarettes and as an effective method of smoking cessation. There are, however, a paucity of data to support these claims. In fact, e-cigarettes are implicated in endothelial dysfunction and oxidative stress in the vasculature and the lungs. The mechanisms underlying these side effects remain unclear. Here, we investigated the effects of e-cigarette vapour on vascular function in smokers and experimental animals to determine the underlying mechanisms.&lt;h4>Methods and results&lt;/h4>Acute e-cigarette smoking produced a marked impairment of endothelial function in chronic smokers determined by flow-mediated dilation. In mice, e-cigarette vapour without nicotine had more detrimental eff</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Jul</publication><modification>2026-05-07T15:11:13.125Z</modification><creation>2022-07-19T16:30:45.112Z</creation></dates><accession>S-EPMC7340357</accession><cross_references><pubmed>31715629</pubmed><doi>10.1093/eurheartj/ehz772</doi></cross_references></HashMap>