Evidence map›Paper›PMID 17272782›Full record

ReviewAmerican journal of respiratory and critical care medicine2007

Bronchopulmonary dysplasia: where have all the vessels gone? Roles of angiogenic growth factors in chronic lung disease.

Bernard Thébaud, Steven H Abman

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

Review in American journal of respiratory and critical care medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 268 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
268citing papers in PubMed, 3 pooled it
20.0field-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

268 citing papers in PubMed, 3 syntheses or guidelines pooled it, 536 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Maternal hypertensive disorders and survival without major morbidities among extremely low gestation newborns.Journal of perinatology : official journal of the California Perinatal Association · 2023
    Trial
  6. Review
  7. Lifelong hypoxia produces multigenerational developmental lung disease and pulmonary hypertension in mice.American journal of physiology. Lung cellular and molecular physiology · 2026
    Article
  8. Left ventricular diastolic dysfunction in preterm infants with bronchopulmonary dysplasia.Journal of perinatology : official journal of the California Perinatal Association · 2026
    Article
  9. Article
  10. Article
  11. Review
  12. Toward precision for bronchopulmonary dysplasia: Moving past current definitions.Journal of perinatology : official journal of the California Perinatal Association · 2026
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
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  20. Article

208 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 2 countries.

Bernard ThébaudDepartment of Pediatrics, Division of Neonatology, Vascular Biology Group, University of Alberta, HMRC 407, Edmonton, AB, T6G 2S2, Canada. bthebaud@ualberta.ca
Steven H Abman
Children's Hospital Colorado · USUniversity of Alberta · CA

Funding

Role of VEGF in Perinatal Pulmonary HypertensionR01HL068702 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI ABMAN, STEVEN HERBERT, SHEPHERD, DOUGLAS · 2001 to 2021
$6.7M
NHLBI NIH HHS R01HL68702
6 · The paper itself

Abstract

Bronchopulmonary dysplasia and emphysema are significant global health problems at the extreme stages of life. Both are characterized by arrested alveolar development or loss of alveoli, respectively. Both lack effective treatment strategies. Knowledge about the genetic control of branching morphogenesis in mammals derives from investigations of the respiratory system in Drosophila, but mechanisms that regulate alveolar development remain poorly understood. Even less is known about regulation of the growth and development of the pulmonary vasculature. Understanding how alveoli and the underlying capillary network develop, and how these mechanisms are disrupted in disease states, are critical for developing effective therapies for lung diseases characterized by impaired alveolar structure. Recent observations have challenged old notions that the development of the blood vessels in the lung passively follows that of the airways. Rather, increasing evidence suggests that lung blood vessels actively promote alveolar growth during development and contribute to the maintenance of alveolar structures throughout postnatal life. Our working hypothesis is that disruption of angiogenesis impairs alveolarization, and that preservation of vascular growth and endothelial survival promotes growth and sustains the architecture of the distal airspace. Furthermore, the explosion of interest in stem cell biology suggests potential roles for endothelial progenitor cells in the pathogenesis or treatment of lung vascular disease. In this Pulmonary Perspective, we review recent data on the importance of the lung circulation, specifically examining the relationship between dysmorphic vascular growth and impaired alveolarization, and speculate on how these new insights may lead to novel therapeutic strategies for bronchopulmonary dysplasia.

Indexed as

AnimalsBronchopulmonary DysplasiaChronic DiseaseHumansInfant, NewbornLungMorphogenesisNeovascularization, PhysiologicPulmonary AlveoliReceptors, Vascular Endothelial Growth FactorStem CellsVascular Endothelial Growth FactorsReceptors, Vascular Endothelial Growth FactorVascular Endothelial Growth Factors

Identifiers

PMID17272782
PMCPMC2176086
OpenAlexW2001065358

What OpenQuestion holds

Textmetadata
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.