Evidence map›Paper›PMID 36290742›Full record

ArticleAntioxidants (Basel, Switzerland)2022

Cigarette Smoke Impairs Airway Epithelial Wound Repair: Role of Modulation of Epithelial-Mesenchymal Transition Processes and Notch-1 Signaling.

Serena Di Vincenzo, Dennis K Ninaber, Chiara Cipollina, Maria Ferraro, Pieter S Hiemstra, Elisabetta Pace

Open access · goldAbstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Lung disease in rheumatoid arthritis.Nature reviews. Rheumatology · 2026
    Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Acute exposure to electronic cigarette components alters mRNA expression of pre-osteoblasts.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  9. Article
  10. Article
  11. Review
  12. Frontiers in pharmacology · 2024
    Article
  13. 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

6 authors at 2 institutions in 2 countries.

Serena Di VincenzoInstitute of Translational Pharmacology (IFT), National Research Council of Italy (CNR), Via Ugo La Malfa, 153, 90146 Palermo, Italy.ORCID 0000-0003-1695-9307
Dennis K NinaberDepartment of Pulmonology, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands.
Chiara CipollinaInstitute of Translational Pharmacology (IFT), National Research Council of Italy (CNR), Via Ugo La Malfa, 153, 90146 Palermo, Italy.
Maria FerraroInstitute of Translational Pharmacology (IFT), National Research Council of Italy (CNR), Via Ugo La Malfa, 153, 90146 Palermo, Italy.
Pieter S HiemstraDepartment of Pulmonology, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands.ORCID 0000-0002-0238-5982
Elisabetta PaceInstitute of Translational Pharmacology (IFT), National Research Council of Italy (CNR), Via Ugo La Malfa, 153, 90146 Palermo, Italy.ORCID 0000-0003-1141-9010
Istituto di Farmacologia Traslazionale · ITLeiden University Medical Center · NL

Funding

Leiden University Medical Center without a specific grant numberNational Research Council without a specific grant number
6 · The paper itself

Abstract

Cigarette smoke (CS) induces oxidative stress and chronic inflammation in airway epithelium. It is a major risk factor for respiratory diseases, characterized by epithelial injury. The impact of CS on airway epithelial repair, which involves epithelial-mesenchymal transition (EMT) and the Notch-1 pathway, is incompletely understood. In this study, we used primary bronchial epithelial cells (PBECs) to evaluate the effect of CS on epithelial repair and these mechanisms. The effect of CS and/or TGF-beta1 on wound repair, various EMT and Notch-1 pathway markers and epithelial cell markers (TP63, SCGB1A) was assessed in PBECs cultured submerged, at the air-liquid interface (ALI) alone and in co-culture with fibroblasts. TGF-beta1 increased epithelial wound repair, activated EMT (shown by decrease in E-cadherin, and increases in vimentin, SNAIL1/SNAIL2/ZEB1), and increased Notch-1 pathway markers (NOTCH1/JAGGED1/HES1), MMP9, TP63, SCGB1A1. In contrast, CS decreased wound repair and vimentin, NOTCH1/JAGGED1/HES1, MMP9, TP63, SCGB1A1, whereas it activated the initial steps of the EMT (decrease in E-cadherin and increases in SNAIL1/SNAIL2/ZEB1). Using combined exposures, we observed that CS counteracted the effects of TGF-beta1. Furthermore, Notch signaling inhibition decreased wound repair. These data suggest that CS inhibits the physiological epithelial wound repair by interfering with the normal EMT process and the Notch-1 pathway.

Indexed as

cigarette smokeepithelial-mesenchymal transitionNotch-1 pathwayproximal airwaysrepair processesTGF-beta1

Identifiers

PMID36290742
PMCPMC9598207
OpenAlexW4304762080

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.