Evidence map›Paper›PMID 40453633›Full record

ArticleTobacco induced diseases2025

Inflammatory response to chronic nicotine-containing electronic cigarette exposure in a rat model of myocardial infarction.

Jianru Shi, Wangde Dai, Juan Carreno, Jaspreet Sachdeva, Jesus Chavez, Michael T Kleinman, David A Herman, Rebecca J Arechavala, Irene Hasen, Amanda Ting and 1 more

Abstract read
In one paragraph

Article in Tobacco induced diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

11 authors.

Jianru ShiCardiovascular Research Institute, Huntington Medical Research Institutes, Pasadena, United States.
Wangde DaiCardiovascular Research Institute, Huntington Medical Research Institutes, Pasadena, United States.
Juan CarrenoCardiovascular Research Institute, Huntington Medical Research Institutes, Pasadena, United States.
Jaspreet SachdevaCardiovascular Research Institute, Huntington Medical Research Institutes, Pasadena, United States.
Jesus ChavezCardiovascular Research Institute, Huntington Medical Research Institutes, Pasadena, United States.
Michael T KleinmanDepartment of Environmental and Occupational Health, University of California Irvine, Irvine, United States.
David A HermanDepartment of Environmental and Occupational Health, University of California Irvine, Irvine, United States.
Rebecca J ArechavalaDepartment of Environmental and Occupational Health, University of California Irvine, Irvine, United States.
Irene HasenDepartment of Environmental and Occupational Health, University of California Irvine, Irvine, United States.
Amanda TingDepartment of Environmental and Occupational Health, University of California Irvine, Irvine, United States.
Robert A KlonerCardiovascular Research Institute, Huntington Medical Research Institutes, Pasadena, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe long-term effects of chronic electronic cigarette (e-cigarette) exposure on lung and heart inflammation during the healing phase of myocardial infarction (MI) remain unexplored. Additionally, the impact of e-cigarette exposure on blood parameters in this context is unclear. This study aims to assess e-cigarette with nicotine (e-cig Nic+) effects on lung histology, inflammatory gene expression in cardiac tissue, and blood parameters during MI recovery.

methodsSprague Dawley rats of both sexes underwent proximal left coronary artery occlusion to induce a large anterior wall MI. After one week, rats were randomized to either air or e-cig Nic+ exposure for 12 weeks.

resultsIn the lungs, e-cig Nic+ exposure led to a significant accumulation of inflammatory cells within the alveolar spaces and increased inflammatory cell numbers in the lung parenchyma compared to the air group. Numerically elevated levels of malondialdehyde (MDA), an oxidative stress biomarker, were observed in the e-cig Nic+ group. In the heart, a PCR array analysis of inflammatory cytokines and receptors revealed that 70 out of 84 inflammatory-related genes were downregulated in the e-cig Nic+ group, with 11 reaching statistical significance. Additionally, the blood of rats exposed to e-cig Nic+ exhibited significantly lower white blood cell, lymphocyte, and platelet counts compared to the air group.

conclusionsChronic exposure to e-cig Nic+ exacerbates lung inflammation, alters inflammatory gene expression in the heart, and suppresses immune cell counts in the blood during MI recovery. These findings suggest that e-cigarette with nicotine aerosol inhalation contributes to lung lesions and dampens immune and inflammatory responses in an already compromised MI setting.

Indexed as

blood parameterscardiac inflammatory genese-cigarettelung inflammation

Identifiers

PMID40453633
PMCPMC12125711

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.