Evidence map›Paper›PMID 22125178›Full record

ReviewBirth defects research. Part A, Clinical and molecular teratology2012

Aberrant signaling pathways of the lung mesenchyme and their contributions to the pathogenesis of bronchopulmonary dysplasia.

Shawn K Ahlfeld, Simon J Conway

Open access · greenAbstract readReview
In one paragraph

Review in Birth defects research. Part A, Clinical and molecular teratology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.0field-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

32 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Hedgehog and Platelet-derived Growth Factor Signaling Intersect during Postnatal Lung Development.American journal of respiratory cell and molecular biology · 2023
    Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Fra-2 negatively regulates postnatal alveolar septation by modulating myofibroblast function.American journal of physiology. Lung cellular and molecular physiology · 2017
    Article
  15. Article
  16. The innate immune response in fetal lung mesenchymal cells targets VEGFR2 expression and activity.American journal of physiology. Lung cellular and molecular physiology · 2017
    Article
  17. Article
  18. Article
  19. Review
  20. Maternal/neonatal vitamin D deficiency: a risk factor for bronchopulmonary dysplasia in preterms?Journal of perinatology : official journal of the California Perinatal Association · 2015
    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

2 authors at 2 institutions in 1 country.

Shawn K AhlfeldDevelopmental Biology and Neonatal Medicine Program, H.B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana. skahlfel@iupui.edu
Simon J Conway
Indiana University – Purdue University Indianapolis · USIndiana University School of Medicine

Funding

Quality Assurance and Quality Control Project Management: Improving Submissions and Study Conduct in the Human Subjects Research Prior Approval ProcessUL1TR002529 · NCATS · INDIANA UNIVERSITY INDIANAPOLIS · PI MOE, SHARON M, WIEHE, SARAH ELIZABETH · 2018 to 2022
$27.2M
Indiana Clinical and Translational Sciences InstituteUL1TR001108 · NCATS · INDIANA UNIVERSITY INDIANAPOLIS · PI DENNE, SCOTT C., SHEKHAR, ANANTHA · 2013 to 2017
$23.3M
Indiana Clinical and Translational Science Institute-K12 ProgramKL2RR025760 · NCRR · INDIANA UNIVERSITY INDIANAPOLIS · PI SHEKHAR, ANANTHA · 2008 to 2011
$2.2M
Indiana Clinical and Translational Science Institute-K12 ProgramKL2TR000163 · NCATS · INDIANA UNIVERSITY INDIANAPOLIS · PI SHEKHAR, ANANTHA · 2012 to 2013
$720k
NCATS NIH HHS KL2 TR000163NCATS NIH HHS UL1 TR001108NCRR NIH HHS KL2 RR025760NHLBI NIH HHS L40 HL110357
6 · The paper itself

Abstract

Bronchopulmonary dysplasia (BPD) is a chronic lung disease in infants born extremely preterm, typically before 28 weeks' gestation, characterized by a prolonged need for supplemental oxygen or positive pressure ventilation beyond 36 weeks postmenstrual age. The limited number of autopsy samples available from infants with BPD in the postsurfactant era has revealed a reduced capacity for gas exchange resulting from simplification of the distal lung structure with fewer, larger alveoli because of a failure of normal lung alveolar septation and pulmonary microvascular development. The mechanisms responsible for alveolar simplification in BPD have not been fully elucidated, but mounting evidence suggests that aberrations in the cross-talk between growth factors of the lung mesenchyme and distal airspace epithelium have a key role. Animal models that recapitulate the human condition have expanded our knowledge of the pathology of BPD and have identified candidate matrix components and growth factors in the developing lung that are disrupted by conditions that predispose infants to BPD and interfere with normal vascular and alveolar morphogenesis. This review focuses on the deviations from normal lung development that define the pathophysiology of BPD and summarizes the various candidate mesenchyme-associated proteins and growth factors that have been identified as being disrupted in animal models of BPD. Finally, future areas of research to identify novel targets affected in arrested lung development and recovery are discussed.

Indexed as

Signal TransductionAnimalsBronchopulmonary DysplasiaHumansInfant, NewbornInfant, PrematureInfant, Premature, DiseasesIntercellular Signaling Peptides and ProteinsLungMesodermMiceProteinsIntercellular Signaling Peptides and ProteinsProteins

Identifiers

PMID22125178
PMCPMC3256283
OpenAlexW2052025430

What OpenQuestion holds

Textmetadata
LicenceTDM
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.