Evidence map›Paper›PMID 28256533›Full record

ArticleScientific reports2017

Myofibroblast differentiation and its functional properties are inhibited by nicotine and e-cigarette via mitochondrial OXPHOS complex III.

Wei Lei, Chad Lerner, Isaac K Sundar, Irfan Rahman

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
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  7. Brain Energy Metabolism in Ischemic Stroke: Effects of Smoking and Diabetes.International journal of molecular sciences · 2022
    Review
  8. Article
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  11. Review
  12. Article
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  15. Reactive Oxygen Species, Mitochondrial Membrane Potential, and Cellular Membrane Potential Are Predictors of E-Liquid Induced Cellular Toxicity.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2020
    Article
  16. Article
  17. Review
  18. Review
  19. 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

4 authors at 2 institutions in 2 countries.

Wei LeiDepartment of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, USA.
Chad LernerDepartment of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, USA.
Isaac K SundarDepartment of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, USA.
Irfan RahmanDepartment of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, USA.
University of Rochester Medical Center · USFirst Affiliated Hospital of Soochow University · CN

Funding

MECHANISMS OF CIGARETTE SMOKE-INDUCED LUNG CELLULAR SENESCENCER01HL085613 · NHLBI · UNIVERSITY OF ROCHESTER · PI RAHMAN, IRFAN · 2007 to 2017
$4.0M
Inflammatory and Dysregulated Repair Responses to Inhaled NicotineR01HL135613 · NHLBI · UNIVERSITY OF ROCHESTER · PI RAHMAN, IRFAN · 2017 to 2021
$2.7M
NHLBI NIH HHS R01 HL085613NHLBI NIH HHS R01 HL135613
6 · The paper itself

Abstract

Nicotine is the major stimulant in tobacco products including e-cigarettes. Fibroblast to myofibroblast differentiation is a key process during wound healing and is dysregulated in lung diseases. The role of nicotine and e-cigarette derived nicotine on cellular functions including profibrotic response and other functional aspects is not known. We hypothesized that nicotine and e-cigarettes affect myofibroblast differentiation, gel contraction, and wound healing via mitochondria stress through nicotinic receptor-dependent mechanisms. To test the hypothesis, we exposed human lung fibroblasts with various doses of nicotine and e-cigarette condensate and determined myofibroblast differentiation, mitochondrial oxidative phosphorylation (OXPHOS), wound healing, and gel contraction at different time points. We found that both nicotine and e-cigarette inhibit myofibroblast differentiation as shown by smooth muscle actin and collagen type I, alpha 1 abundance. Nicotine and e-cigarette inhibited OXPHOS complex III accompanied by increased MitoROS, and this effect was augmented by complex III inhibitor antimycin A. These mitochondrial associated effects by nicotine resulted in inhibition of myofibroblast differentiation. These effects were associated with inhibition of wound healing and gel contraction suggesting that nicotine is responsible for dysregulated repair during injurious responses. Thus, our data suggest that nicotine causes dysregulated repair by inhibition of myofibroblast differentiation via OXPHOS pathway.

Indexed as

Cell DifferentiationCells, CulturedElectronic Nicotine Delivery SystemsElectron Transport Complex IIIHumansMitochondriaMyofibroblastsNicotineOxidative PhosphorylationReactive Oxygen SpeciesElectron Transport Complex IIINicotineReactive Oxygen Species

Identifiers

PMID28256533
PMCPMC5335673
OpenAlexW2593640202

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.