Evidence map›Paper›PMID 24739494›Full record

ReviewCurrent opinion in pediatrics2014

Disrupted lung development and bronchopulmonary dysplasia: opportunities for lung repair and regeneration.

Christopher D Baker, Cristina M Alvira

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Current opinion in pediatrics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 3 pooled it
6.8field-weighted citation impact, top 3% 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

68 citing papers in PubMed, 3 syntheses or guidelines pooled it, 111 citations in OpenAlex.

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  7. Review
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  11. Effect of vitamin D supplementation on incidence of bronchopulmonary dysplasia among preterm infants up to 36 weeks' gestational age.Nutrition in clinical practice : official publication of the American Society for Parenteral and Enteral Nutrition · 2025
    Review
  12. Article
  13. Observational
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8 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Christopher D BakeraSection of Pulmonary Medicine and Pediatric Heart Lung Center, Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado, USA bDepartment of Pediatrics, Center for Excellence in Pulmonary Biology, Stanford University School of Medicine, Stanford, California, USA.
Cristina M Alvira
Stanford University · US

Funding

Colorado Clinical and Translational Sciences InstituteUL1TR001082 · NCATS · UNIVERSITY OF COLORADO DENVER · PI SOKOL, RONALD J. · 2013 to 2017
$48.0M
Novel Molecular Mechanisms Regulating Postnatal Pulmonary AngiogenesisR01HL122918 · NHLBI · STANFORD UNIVERSITY · PI ALVIRA, CRISTINA MARIA · 2014 to 2018
$2.3M
Colorado Career Development Program in the Genetics and Genomics of Lung DiseasesK12HL090147 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI GERACI, MARK W · 2007 to 2012
$2.0M
Postnatal Lung Development: Mechanisms of Molecular and Vascular DevelopmentP30HL101315 · NHLBI · STANFORD UNIVERSITY · PI CORNFIELD, DAVID N. · 2009 to 2010
$1.6M
NCATS NIH HHS UL1 TR001082NHLBI NIH HHS 1P30HL101315-01NHLBI NIH HHS K12 HL090147NHLBI NIH HHS K12-HL090147-01NHLBI NIH HHS P30 HL101315NHLBI NIH HHS R01 HL122918
6 · The paper itself

Abstract

purpose of reviewAdvances in medical therapy have increased survival of extremely premature infants and changed the pathology of bronchopulmonary dysplasia (BPD) from one of acute lung injury to a disease of disrupted lung development. With this evolution, new questions emerge regarding the molecular mechanisms that control postnatal lung development, the effect of early disruptions of postnatal lung development on long-term lung function, and the existence of endogenous mechanisms that permit lung regeneration after injury. RECENT

findingsRecent data demonstrate that a significant component of alveolarization, the final stage of lung development, occurs postnatally. Further, clinical and experimental studies demonstrate that premature birth disrupts alveolarization, decreasing the gas exchange surface area of the lung and causing BPD. BPD is associated with significant short-term morbidity, and new longitudinal, clinical data demonstrate that survivors of BPD have long-standing deficits in lung function and may be at risk for the development of additional lung disease as adults. Unfortunately, current care is mainly supportive with few effective therapies that prevent or treat established BPD. These studies underscore the need to further elucidate the mechanisms that direct postnatal lung growth and develop innovative strategies to stimulate lung regeneration. SUMMARY: Despite significant improvements in the care and survival of extremely premature infants, BPD remains a major clinical problem. Although efforts should remain focused on the prevention of preterm labor and BPD, novel research aimed at promoting postnatal alveolarization offers a unique opportunity to develop effective strategies to treat established BPD.

Indexed as

OrganogenesisRegenerationBronchopulmonary DysplasiaHumansInfant, Extremely PrematureInfant, NewbornLungMolecular Targeted TherapySurvival Analysis

Identifiers

PMID24739494
PMCPMC4121955
OpenAlexW1974089041

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.