Evidence map›Paper›PMID 40703064›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2025

Chronic Pod-Mod E-Cigarette Aerosol Exposure Induces Aortic Dysfunction in Hypercholesterolemic Mice: Role of Oxidative Stress and Inflammation.

Yasmeen M Farra, Simone Sabnis, Jacqueline Matz, Hannah I B Wilker, Victoria A Williams, Oliver Trejo, Hannah Kim, Cristobal F Rivera, John Vlahos, Bhama Ramkhelawon and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Yasmeen M FarraDepartment of Bioengineering, Northeastern University, Boston, MA (Y.M.F., S.S., J.M., H.I.B.W., V.A.W., O.T., H.K., J.M.O., C.B.).
Simone SabnisDepartment of Bioengineering, Northeastern University, Boston, MA (Y.M.F., S.S., J.M., H.I.B.W., V.A.W., O.T., H.K., J.M.O., C.B.).
Jacqueline MatzDepartment of Bioengineering, Northeastern University, Boston, MA (Y.M.F., S.S., J.M., H.I.B.W., V.A.W., O.T., H.K., J.M.O., C.B.).ORCID 0000-0003-0026-9731
Hannah I B WilkerDepartment of Bioengineering, Northeastern University, Boston, MA (Y.M.F., S.S., J.M., H.I.B.W., V.A.W., O.T., H.K., J.M.O., C.B.).
Victoria A WilliamsDepartment of Bioengineering, Northeastern University, Boston, MA (Y.M.F., S.S., J.M., H.I.B.W., V.A.W., O.T., H.K., J.M.O., C.B.).ORCID 0009-0000-7683-9564
Oliver TrejoDepartment of Bioengineering, Northeastern University, Boston, MA (Y.M.F., S.S., J.M., H.I.B.W., V.A.W., O.T., H.K., J.M.O., C.B.).ORCID 0009-0004-7234-3253
Hannah KimDepartment of Bioengineering, Northeastern University, Boston, MA (Y.M.F., S.S., J.M., H.I.B.W., V.A.W., O.T., H.K., J.M.O., C.B.).
Cristobal F RiveraDivision of Vascular and Endovascular Surgery, Department of Surgery (C.F.R., J.V., B.R.), New York University Langone Medical Center, New York City.ORCID 0000-0001-9648-9880
John VlahosDivision of Vascular and Endovascular Surgery, Department of Surgery (C.F.R., J.V., B.R.), New York University Langone Medical Center, New York City.
Bhama RamkhelawonDivision of Vascular and Endovascular Surgery, Department of Surgery (C.F.R., J.V., B.R.), New York University Langone Medical Center, New York City.ORCID 0000-0002-9087-0995
Jessica M OakesDepartment of Bioengineering, Northeastern University, Boston, MA (Y.M.F., S.S., J.M., H.I.B.W., V.A.W., O.T., H.K., J.M.O., C.B.).ORCID 0000-0001-9669-0680
Chiara BelliniDepartment of Bioengineering, Northeastern University, Boston, MA (Y.M.F., S.S., J.M., H.I.B.W., V.A.W., O.T., H.K., J.M.O., C.B.).ORCID 0000-0003-0823-4613

Funding

Spatiotemporal checkpoints of macrophages in aortic aneurysms- RenewalR01HL146627 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Bhama Ramkhelawon · 2019 to 2026
$6.1M
Cardiopulmonary outcomes of dual cigarette and e-cigarette use in animal models of chronic exposureR01HL168719 · NHLBI · NORTHEASTERN UNIVERSITY · PI Chiara Bellini · 2023 to 2026
$3.1M
Origin and Immune Functions of Platelets in Aortic AneurysmsR01HL149927 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RAMKHELAWON, BHAMA · 2020 to 2023
$2.4M
Pulmonary and Cardiovascular Health Consequences Following Electronic Cigarette ExposureR03HL142472 · NHLBI · NORTHEASTERN UNIVERSITY · PI BELLINI, CHIARA, OAKES, JESSICA M · 2018 to 2019
$157k
NHLBI NIH HHS R01 HL146627NHLBI NIH HHS R01 HL149927NHLBI NIH HHS R01 HL168719NHLBI NIH HHS R03 HL142472
6 · The paper itself

Abstract

backgroundElectronic cigarettes (e-cigarettes) are the most used tobacco product among youth, and adults who smoke combustible cigarettes favor e-cigarettes over approved cessation aids. Despite the lower perceived harm of vaping compared with smoking, acute inhalation of e-cigarette aerosol elicits cardiovascular responses that may lead to persistent damage when repeated over time.

methodsWe exposed female hypercholesterolemic mice to either pod-mod e-cigarette aerosol or filtered air daily for 24 weeks. We assessed the long-term effects of vaping on aortic stiffness and vasoreactivity while investigating the underlying cellular and molecular mechanisms of injury.

resultsChronic inhalation of e-cigarette aerosol triggered the accumulation of inflammatory signals systemically and within aortic tissues, as well as T-lymphocyte accrual in the aortic wall. Limited eNOS (endothelial nitric oxide synthase) expression and enhanced superoxide radical production curbed NO bioavailability in the aorta of mice exposed to e-cigarette aerosol despite iNOS (inducible nitric oxide synthase) induction, impairing the endothelium-dependent vasodilation that regulates blood flow distribution. Inhalation of e-cigarette aerosol thickened and stiffened aortic tissues via collagen deposition and remodeling, hindering the storage of elastic energy and limiting the cyclic distensibility that enables the aorta to function as a pressure reservoir. These effects combined contributed to raising systolic and pulse pressure above control levels.

conclusionsChronic inhalation of aerosol from pod-mod e-cigarettes promotes oxidative stress, inflammation, and fibrosis within aortic tissues, significantly impairing passive and vasoactive aortic functions. This evidence provides new insights into the biological processes that increase the risk of adverse cardiovascular events as a result of pod-mod e-cigarette vaping.

Indexed as

AortaAortic DiseasesE-Cigarette VaporElectronic Nicotine Delivery SystemsHypercholesterolemiaInflammationOxidative StressVapingAerosolsAnimalsDisease Models, AnimalFemaleInflammation MediatorsMiceMice, Inbred C57BLNitric OxideAerosolsE-Cigarette VaporInflammation MediatorsNitric OxideNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINos2 protein, mouseNos3 protein, mouseaortic stiffnesscytokineselectronic nicotine delivery systemfibrosisreactive oxygen speciesvasodilation

Identifiers

PMID40703064
PMCPMC12370285

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.