Evidence map›Paper›PMID 35445327›Full record

ReviewMolecular and cellular pediatrics2022

When inflammation meets lung development-an update on the pathogenesis of bronchopulmonary dysplasia.

Lena Holzfurtner, Tayyab Shahzad, Ying Dong, Lisa Rekers, Ariane Selting, Birte Staude, Tina Lauer, Annesuse Schmidt, Stefano Rivetti, Klaus-Peter Zimmer and 3 more

Open access · goldAbstract readReview
In one paragraph

Review in Molecular and cellular pediatrics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 3 pooled it
9.0field-weighted citation impact, top 1% 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

56 citing papers in PubMed, 3 syntheses or guidelines pooled it, 60 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  4. Trial
  5. Review
  6. Article
  7. LncRNA SNHG14 drives alveolar inflammation in bronchopulmonary dysplasia via DNMT3a-mediated epigenetic silencing of miR-214-3p.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  8. Article
  9. Article
  10. TLR9-mediated innate immune signaling contributes to acetaminophen-induced injury in the developing lung.American journal of physiology. Lung cellular and molecular physiology · 2026
    Article
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  17. Observational
  18. The Developmental Origins of Asthma and COPD.Annual review of physiology · 2026
    Review
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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

13 authors at 2 institutions in 1 country.

Lena Holzfurtner *Department of General Pediatrics and Neonatology, Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Justus-Liebig-University, Feulgenstrasse 12, 35392, Giessen, Germany.
Tayyab Shahzad *Department of General Pediatrics and Neonatology, Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Justus-Liebig-University, Feulgenstrasse 12, 35392, Giessen, Germany.
Ying DongDepartment of General Pediatrics and Neonatology, Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Justus-Liebig-University, Feulgenstrasse 12, 35392, Giessen, Germany.
Lisa RekersDepartment of General Pediatrics and Neonatology, Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Justus-Liebig-University, Feulgenstrasse 12, 35392, Giessen, Germany.
Ariane SeltingDepartment of General Pediatrics and Neonatology, Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Justus-Liebig-University, Feulgenstrasse 12, 35392, Giessen, Germany.
Birte StaudeDepartment of General Pediatrics and Neonatology, Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Justus-Liebig-University, Feulgenstrasse 12, 35392, Giessen, Germany.
Tina LauerDepartment of General Pediatrics and Neonatology, Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Justus-Liebig-University, Feulgenstrasse 12, 35392, Giessen, Germany.
Annesuse SchmidtDepartment of General Pediatrics and Neonatology, Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Justus-Liebig-University, Feulgenstrasse 12, 35392, Giessen, Germany.
Stefano RivettiDepartment of Internal Medicine II, Universities of Giessen and Marburg Lung Center (UGMLC), Cardiopulmonary Institute (CPI), Member of the German Center for Lung Research (DZL), Justus-Liebig-University, Aulweg 130, 35392, Giessen, Germany.
Klaus-Peter ZimmerDepartment of General Pediatrics and Neonatology, Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Justus-Liebig-University, Feulgenstrasse 12, 35392, Giessen, Germany.
Judith BehnkeDepartment of General Pediatrics and Neonatology, Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Justus-Liebig-University, Feulgenstrasse 12, 35392, Giessen, Germany.
Saverio BellusciDepartment of Internal Medicine II, Universities of Giessen and Marburg Lung Center (UGMLC), Cardiopulmonary Institute (CPI), Member of the German Center for Lung Research (DZL), Justus-Liebig-University, Aulweg 130, 35392, Giessen, Germany.
Harald EhrhardtDepartment of General Pediatrics and Neonatology, Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Justus-Liebig-University, Feulgenstrasse 12, 35392, Giessen, Germany. Harald.Ehrhardt@paediat.med.uni-giessen.de.ORCID http://orcid.org/0000-0003-4587-1734
Universities of Giessen and Marburg Lung Center · DEGerman Center for Lung Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Even more than 50 years after its initial description, bronchopulmonary dysplasia (BPD) remains one of the most important and lifelong sequelae following premature birth. Tremendous efforts have been undertaken since then to reduce this ever-increasing disease burden but a therapeutic breakthrough preventing BPD is still not in sight. The inflammatory response provoked in the immature lung is a key driver of distorted lung development and impacts the formation of alveolar, mesenchymal, and vascular structures during a particularly vulnerable time-period. During the last 5 years, new scientific insights have led to an improved pathomechanistic understanding of BPD origins and disease drivers. Within the framework of current scientific progress, concepts involving disruption of the balance of key inflammatory and lung growth promoting pathways by various stimuli, take center stage. Still today, the number of efficient therapeutics available to prevent BPD is limited to a few, well-established pharmacological interventions including postnatal corticosteroids, early caffeine administration, and vitamin A. Recent advances in the clinical care of infants in the neonatal intensive care unit (NICU) have led to improvements in survival without a consistent reduction in the incidence of BPD. Our update provides latest insights from both preclinical models and clinical cohort studies and describes novel approaches to prevent BPD.

Indexed as

Bronchopulmonary dysplasiaChronic lung diseaseInflammationLung injuryPretermReactive oxygen speciesRodentTherapeutic approach

Identifiers

PMID35445327
PMCPMC9021337
OpenAlexW4224291887

What Socratic 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 Socratic graph.