Evidence map›Paper›PMID 32331221›Full record

ReviewCells2020

Nicotine in Senescence and Atherosclerosis.

Ann Marie Centner, Pradeep G Bhide, Gloria Salazar

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

37 citing papers in PubMed, 73 citations in OpenAlex.

  1. Trial
  2. Article
  3. Senolytics Reverse PMCardiovascular toxicology · 2026
    Article
  4. CIITA/PRMT5 promote CD4BMC medicine · 2026
    Article
  5. Article
  6. Review
  7. Observational
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Rational Design of a Flavoenzyme for Aerobic Nicotine Catabolism.bioRxiv : the preprint server for biology · 2024
    Article
  18. Review
  19. Cardiovascular dysfunction induced by combined exposure to nicotine inhalation and high-fat diet.American journal of physiology. Heart and circulatory physiology · 2024
    Article
  20. 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

3 authors at 1 institution in 1 country.

Ann Marie CentnerDepartment of Nutrition, Food and Exercise Sciences, College of Human Scinces, 120 Convocation Way, Florida State University, Tallahassee, FL 32306, USA.
Pradeep G BhideDepartment of Biomedical Sciences, FSU College of Medicine, 1115, West Call Street, Tallahassee, FL 32306, USA.ORCID 0000-0003-4236-9415
Gloria SalazarDepartment of Nutrition, Food and Exercise Sciences, College of Human Scinces, 120 Convocation Way, Florida State University, Tallahassee, FL 32306, USA.ORCID 0000-0002-6239-7942
Florida State University · US

Funding

Transgenerational Transmission of the Effects of Paternal Nicotine ExposureR15DA043848 · NIDA · FLORIDA STATE UNIVERSITY · PI BHIDE, PRADEEP G · 2018 to 2018
$459k
NIDA NIH HHS R15 DA043848
6 · The paper itself

Abstract

Cigarette smoke is a known exacerbator of age-related pathologies, such as cardiovascular disease (CVD), atherosclerosis, and cellular aging (senescence). However, the role of nicotine and its major metabolite cotinine is yet to be elucidated. Considering the growing amount of nicotine-containing aerosol use in recent years, the role of nicotine is a relevant public health concern. A number of recent studies and health education sites have focused on nicotine aerosol-induced adverse lung function, and neglected cardiovascular (CV) impairments and diseases. A critical review of the present scientific literature leads to the hypothesis that nicotine mediates the effects of cigarette smoke in the CV system by increasing MAPK signaling, inflammation, and oxidative stress through NADPH oxidase 1 (Nox1), to induce vascular smooth muscle cell (VSMC) senescence. The accumulation of senescent VSMCs in the lesion cap is detrimental as it increases the pathogenesis of atherosclerosis by promoting an unstable plaque phenotype. Therefore, nicotine, and most likely its metabolite cotinine, adversely influence atherosclerosis.

Indexed as

Cellular SenescenceAnimalsAtherosclerosisCardiovascular SystemDisease Models, AnimalHumansNicotineTobacco UseNicotineApoE−/−atherosclerosiscigarette smokecotininenicotinesenescenceVSMC

Identifiers

PMID32331221
PMCPMC7226537
OpenAlexW3017455379

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.