Evidence map›Paper›PMID 37552822›Full record

ArticleAmerican journal of respiratory cell and molecular biology2023

Overactivated Epithelial NF-κB Disrupts Lung Development in Congenital Diaphragmatic Hernia.

Florentine Dylong, Jan Riedel, Gaurang M Amonkar, Nicole Peukert, Paula Lieckfeldt, Katinka Sturm, Benedikt Höxter, Wai Hei Tse, Yuichiro Miyake, Maria Moormann and 7 more

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Article in American journal of respiratory cell and molecular biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
–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

12 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Mechanical compression causes lung hypoplasia in congenital diaphragmatic hernia with GATA4 genetic variants.American journal of physiology. Lung cellular and molecular physiology · 2026
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. NF-κB Signaling in Congenital Diaphragmatic Hernia: A Potential Therapeutic Strategy?American journal of respiratory cell and molecular biology · 2023
    Article
  12. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors.

Florentine DylongDepartment of Pediatric Surgery, University Hospital Leipzig, Leipzig, Germany.
Jan RiedelDepartment of Pediatric Surgery, University Hospital Leipzig, Leipzig, Germany.
Gaurang M AmonkarDivision of Newborn Medicine, Department of Pediatrics, Massachusetts General Hospital, Boston, Massachusetts; and.
Nicole PeukertDepartment of Pediatric Surgery, University Hospital Leipzig, Leipzig, Germany.
Paula LieckfeldtDepartment of Pediatric Surgery, University Hospital Leipzig, Leipzig, Germany.
Katinka SturmDepartment of Pediatric Surgery, University Hospital Leipzig, Leipzig, Germany.
Benedikt HöxterDepartment of Pediatric Surgery, University Hospital Leipzig, Leipzig, Germany.
Wai Hei TseDepartment of Surgery.
Yuichiro MiyakeDepartment of Surgery.
Maria MoormannDepartment of Pediatric Surgery, University Hospital Leipzig, Leipzig, Germany.
Lena Marie BodeDepartment of Pediatric Surgery, University Hospital Leipzig, Leipzig, Germany.
Steffi MayerDepartment of Pediatric Surgery, University Hospital Leipzig, Leipzig, Germany.
Richard KeijzerDepartment of Surgery.
Martin LacherDepartment of Pediatric Surgery, University Hospital Leipzig, Leipzig, Germany.
Xingbin AiDivision of Newborn Medicine, Department of Pediatrics, Massachusetts General Hospital, Boston, Massachusetts; and.
Jan-Hendrik GosemannDepartment of Pediatric Surgery, University Hospital Leipzig, Leipzig, Germany.
Richard WagnerDepartment of Pediatric Surgery, University Hospital Leipzig, Leipzig, Germany.ORCID 0000-0002-3035-2619

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Abnormal lung development is the main cause of morbidity and mortality in neonates with congenital diaphragmatic hernia (CDH), a common birth defect (1:2,500) of largely unknown pathobiology. Recent studies discovered that inflammatory processes, and specifically NF-κB-associated pathways, are enriched in human and experimental CDH. However, the molecular signaling of NF-κB in abnormal CDH lung development and its potential as a therapeutic target require further investigation. Using sections and hypoplastic lung explant cultures from the nitrofen rat model of CDH and human fetal CDH lungs, we demonstrate that NF-κB and its downstream transcriptional targets are hyperactive during abnormal lung formation in CDH. NF-κB activity was especially elevated in the airway epithelium of nitrofen and human CDH lungs at different developmental stages. Fetal rat lung explants had impaired pseudoglandular airway branching after exposure to nitrofen, together with increased phosphorylation and transcriptional activity of NF-κB. Dexamethasone, the broad and clinically applicable antiinflammatory NF-κB antagonist, rescued lung branching and normalized NF-κB signaling in hypoplastic lung explants. Moreover, specific NF-κB inhibition with curcumenol similarly rescued

Indexed as

Hernias, Diaphragmatic, CongenitalLung DiseasesAnimalsDexamethasoneDisease Models, AnimalFemaleHumansLungNF-kappa BPhenyl EthersPregnancyRatsRats, Sprague-DawleyDexamethasoneNF-kappa BnitrofenPhenyl EthersCDHlung hypoplasiaNF-κBnitrofen rat modelprenatal inflammation

Identifiers

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Registered trials

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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.