Pitfalls, Problems, and Progress in Bronchopulmonary Dysplasia

Bhandari, Anita; Bhandari, Vineet

doi:10.1542/peds.2008-1962

Cited by 214 publications

(206 citation statements)

References 188 publications

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“…This can have long-term consequences contributing to the development of bronchopulmonary dysplasia (9). Current revised neonatal resuscitation guidelines recommend starting resuscitation with air for the term and near-term infant, but there is still no consensus on which FiO 2 to administer to the preterm (10).…”

mentioning

confidence: 99%

Transcriptome profiling of the newborn mouse lung after hypoxia and reoxygenation: hyperoxic reoxygenation affects mTOR signaling pathway, DNA repair, and JNK-pathway regulation

et al. 2013

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mentioning

confidence: 99%

Transcriptome profiling of the newborn mouse lung after hypoxia and reoxygenation: hyperoxic reoxygenation affects mTOR signaling pathway, DNA repair, and JNK-pathway regulation

et al. 2013

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“…Over the past four decades, the incidence of this disease has significantly increased as a result of improved survival of extremely-low-birthweight infants (2). The pathology of BPD is increasingly being recognized as a developmental arrest of the immature lung caused by injurious stimuli such as mechanical ventilation, oxygen exposure, and intrauterine or postnatal infections.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of β-catenin signaling protects against CTGF-induced alveolar and vascular pathology in neonatal mouse lung

et al. 2016

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Background: Bronchopulmonary dysplasia (BPD) is the most common and serious chronic lung disease of premature infants. Connective tissue growth factor (CTGF) plays an important role in tissue development and remodeling. We have previously shown that targeted overexpression of CTGF in alveolar type II epithelial cells results in BPD-like pathology and activates β-catenin in neonatal mice. Methods: Utilizing this transgenic mouse model and ICG001, a specific pharmacological inhibitor of β-catenin, we tested the hypothesis that β-catenin signaling mediates the effects of CTGF in the neonatal lung. Newborn CTGF mice and control littermates received ICG001 (10 mg/kg/dose) or placebo (dimethyl sulfoxide, equal volume) by daily i.p. injection from postnatal day 5 to 15. Alveolarization, vascular development, and pulmonary hypertension (PH) were analyzed. results: Administration of ICG001 significantly downregulated expression of cyclin D1, collagen 1a1, and fibronectin, which are the known target genes of β-catenin signaling in CTGF lungs. Inhibition of β-catenin signaling improved alveolar and vascular development and decreased pulmonary vascular remodeling. More importantly, the improved vascular development and vascular remodeling led to a decrease in PH. conclusion: β-Catenin signaling mediates the autocrine and paracrine effects of CTGF in the neonatal lung. Inhibition of CTGF-β-catenin signaling may provide a novel therapy for BPD. INTRODUCTIONBronchopulmonary dysplasia (BPD) is the most common and serious chronic lung disease of premature infants (1). Over the past four decades, the incidence of this disease has significantly increased as a result of improved survival of extremely-low-birthweight infants (2). The pathology of BPD is increasingly being recognized as a developmental arrest of the immature lung caused by injurious stimuli such as mechanical ventilation, oxygen exposure, and intrauterine or postnatal infections. Larger and simplified alveoli, decreased vascular growth, and variable interstitial fibrosis are the key pathological features observed in lungs of infants who died of BPD (1). The combination of decreased vascular growth and excessive pulmonary vascular remodeling leads to pulmonary hypertension (PH) which significantly contributes to the morbidity and mortality of these infants (3). Yet, the underlying cellular and molecular mechanisms are poorly defined, and there is no effective therapy.Connective tissue growth factor (CTGF) is a matricellular protein that plays an important role in tissue development and remodeling (4). Recent studies have highlighted the potential role of CTGF in BPD development and progression. The clinical association of CTGF with BPD is best established by studies demonstrating increased CTGF concentrations in bronchoalveolar lavage fluid from preterm infants developing BPD (5) and increased CTGF expression in lung tissues of infants who died of BPD (6). Multiple studies have examined the potential role of CTGF in experimental BPD and demonstrated that increased CTG...

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“…Así, fue posible abordar un interrogante que ha generado controversia en los últimos años: ¿cuál es la mejor opción de tratamiento para los recién nacidos con déficit de surfactante, en quienes la opción de aplicarlo de manera suplementaria implica recurrir al soporte respiratorio con métodos invasivos o con alternativas no invasivas, pues esta conducta influye claramente en los resultados? (1,5,(15)(16)(17)(18)(19)(20)(21)(22)(23)(24).…”

Section: Discussionunclassified

“…Estos resultados se unen a los de muchas otras series citadas en la literatura científica, en las que se ha encontrado que la CPAP disminuye la incidencia de displasia broncopulmonar (3,4,(6)(7)(8)18,19,21,24,32,33). En otros estudios no se han encontrado diferencias en la incidencia de la displasia broncopulmonar, pero en ninguno de ellos se empleó la misma intervención evaluada en el presente estudio.…”

Section: Discussionunclassified

Nasal CPAP vs. mechanical ventilation in 28-32 weeks preterm infants with early surfactant administration

et al. 2014

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Pitfalls, Problems, and Progress in Bronchopulmonary Dysplasia

Cited by 214 publications

References 188 publications

Transcriptome profiling of the newborn mouse lung after hypoxia and reoxygenation: hyperoxic reoxygenation affects mTOR signaling pathway, DNA repair, and JNK-pathway regulation

Transcriptome profiling of the newborn mouse lung after hypoxia and reoxygenation: hyperoxic reoxygenation affects mTOR signaling pathway, DNA repair, and JNK-pathway regulation

Inhibition of β-catenin signaling protects against CTGF-induced alveolar and vascular pathology in neonatal mouse lung

Nasal CPAP vs. mechanical ventilation in 28-32 weeks preterm infants with early surfactant administration

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