Evidence map›Paper›PMID 21239535›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2011

CTGF disrupts alveolarization and induces pulmonary hypertension in neonatal mice: implication in the pathogenesis of severe bronchopulmonary dysplasia.

Shaoyi Chen, Min Rong, Astrid Platteau, Dorothy Hehre, Heather Smith, Philip Ruiz, Jeffrey Whitsett, Eduardo Bancalari, Shu Wu

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
–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

40 citing papers in PubMed.

  1. The emerging role of integrin signaling in pulmonary vascular disease.American journal of physiology. Lung cellular and molecular physiology · 2026
    Review
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  3. Loss ofAmerican journal of respiratory cell and molecular biology · 2025
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  4. Review
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  8. Review
  9. Article
  10. Review
  11. Article
  12. EndothelialAntioxidants (Basel, Switzerland) · 2021
    Article
  13. Interactive and independent effects of early lipopolysaccharide and hyperoxia exposure on developing murine lungs.American journal of physiology. Lung cellular and molecular physiology · 2020
    Article
  14. Review
  15. Article
  16. Perinatal maternal antibiotic exposure augments lung injury in offspring in experimental bronchopulmonary dysplasia.American journal of physiology. Lung cellular and molecular physiology · 2020
    Article
  17. Review
  18. Review
  19. Characteristics of Pulmonary Vascular Remodeling in a Novel Model of Shunt-Associated Pulmonary Arterial Hypertension.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  20. 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

9 authors.

Shaoyi ChenDepartment of Pediatrics, Division of Neonatology, Univ. of Miami Miller School of Medicine, FL 33101, USA.
Min Rong
Astrid Platteau
Dorothy Hehre
Heather Smith
Philip Ruiz
Jeffrey Whitsett
Eduardo Bancalari
Shu Wu

Funding

CTGF in Normal and Deranged Lung MorphogenesisK08HD046582 · NICHD · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI WU, SHU · 2005 to 2009
$653k
NICHD NIH HHS K08 HD046582
6 · The paper itself

Abstract

The pathological hallmarks of bronchopulmonary dysplasia (BPD), one of the most common long-term pulmonary complications associated with preterm birth, include arrested alveolarization, abnormal vascular growth, and variable interstitial fibrosis. Severe BPD is often complicated by pulmonary hypertension characterized by excessive pulmonary vascular remodeling and right ventricular hypertrophy that significantly contributes to the mortality and morbidity of these infants. Connective tissue growth factor (CTGF) is a multifunctional protein that coordinates complex biological processes during tissue development and remodeling. We have previously shown that conditional overexpression of CTGF in airway epithelium under the control of the Clara cell secretory protein promoter results in BPD-like architecture in neonatal mice. In this study, we have generated a doxycycline-inducible double transgenic mouse model with overexpression of CTGF in alveolar type II epithelial (AT II) cells under the control of the surfactant protein C promoter. Overexpression of CTGF in neonatal mice caused dramatic macrophage and neutrophil infiltration in alveolar air spaces and perivascular regions. Overexpression of CTGF also significantly decreased alveolarization and vascular development. Furthermore, overexpression of CTGF induced pulmonary vascular remodeling and pulmonary hypertension. Most importantly, we have also demonstrated that these pathological changes are associated with activation of integrin-linked kinase (ILK)/glucose synthesis kinase-3β (GSK-3β)/β-catenin signaling. These data indicate that overexpression of CTGF in AT II cells results in lung pathology similar to those observed in infants with severe BPD and that ILK/GSK-3β/β-catenin signaling may play an important role in the pathogenesis of severe BPD.

Indexed as

AnimalsAnimals, Newbornbeta CateninCell NucleusConnective Tissue Growth FactorGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHypertension, PulmonaryLungLung InjuryMiceModels, BiologicalPhosphorylationPneumoniaPulmonary Alveolibeta CateninCCN2 protein, mouseConnective Tissue Growth FactorGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, mouse

Identifiers

PMID21239535
PMCPMC3064286

What OpenQuestion holds

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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.