Evidence map›Paper›PMID 29236702›Full record

ArticlePloS one2017

Oral nicotine aggravates endothelial dysfunction and vascular inflammation in diet-induced obese rats: Role of macrophage TNFα.

Chang Liu, Ming-Sheng Zhou, Yao Li, Aimei Wang, Kiranmai Chadipiralla, Runxia Tian, Leopoldo Raij

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 10% of its field
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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Nutrients · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. How Electronic Cigarette Affects the Vascular System.Journal of smoking cessation · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
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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

7 authors at 3 institutions in 2 countries.

Chang LiuDepartment of Endocrinology, First Affiliated Hospital, Jinzhou Medical University, Jinzhou, P.R. of China.
Ming-Sheng ZhouDepartment of Physiology, Shenyang Medical University, Shenyang, P.R. of China.ORCID http://orcid.org/0000-0001-9075-345X
Yao LiDepartment of Physiology, Jinzhou Medical University, Jinzhou, P.R. of China.
Aimei WangDepartment of Physiology, Jinzhou Medical University, Jinzhou, P.R. of China.
Kiranmai ChadipirallaNephrology-Hypertension Section, University of Miami Miller School of Medicine, Miami VAMC, Miami, Florida, United States of America.
Runxia TianNephrology-Hypertension Section, University of Miami Miller School of Medicine, Miami VAMC, Miami, Florida, United States of America.
Leopoldo RaijNephrology-Hypertension Section, University of Miami Miller School of Medicine, Miami VAMC, Miami, Florida, United States of America.
Jinzhou Medical University · CNUniversity of Miami · USShenyang Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity and cigarette smoke are major cardiovascular (CV) risk factors and, when coexisting in the same individuals, have additive/synergistic effects upon CVD. We studied the mechanisms involved in nicotine enhancement of CVD in Sprague Dawley rats with diet-induced obesity. The rats were fed either a high fat (HFD) or normal rat chow diet with or without nicotine (100 mg/L in drinking water) for 20 weeks. HFD rats developed central obesity, increased systolic blood pressure (SBP), aortic superoxide (O2-) production, and impaired endothelial nitric oxide synthase (eNOS) and endothelium-dependent relaxation to acetylcholine (EDR). Nicotine further increased SBP, O2- and impaired eNOS and EDR in obese rats. In the peritoneal macrophages from obese rats, tumor necrosis factor (TNF) α, interleukin 1β and CD36 were increased, and were further increased in nicotine-treated obese rats. Using PCR array we found that 3 of 84 target proinflammatory genes were increased by 2-4 fold in the aorta of obese rats, 11 of the target genes were further increased in nicotine-treated obese rats. HUVECs, incubated with conditioned medium from the peritoneal macrophages of nicotine treated-obese rats, exhibited reduced eNOS and increased NADPH oxidase subunits gp91phox and p22phox expression. Those effects were partially prevented by adding anti-TNFα antibody to the conditioned medium. Our results suggest that nicotine aggravates the CV effects of diet-induced obesity including the oxidative stress, vascular inflammation and endothelial dysfunction. The underlying mechanisms may involve in targeting endothelium by enhancement of macrophage-derived TNFα.

Indexed as

Administration, OralAnimalsBlood PressureBody WeightCotinineC-Reactive ProteinDiet, High-FatEndothelium, VascularMacrophages, PeritonealMaleNicotineObesityRatsRats, Sprague-DawleyReactive Oxygen SpeciesReal-Time Polymerase Chain ReactionCotinineC-Reactive ProteinNicotineReactive Oxygen SpeciesTumor Necrosis Factor-alpha

Identifiers

PMID29236702
PMCPMC5728478
OpenAlexW2774588923

What OpenQuestion holds

Textmetadata
LicenceCC0
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.