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Recent advances in antenatal factors predisposing to bronchopulmonary dysplasia
Elizabeth Taglauer1, Steven H Abman2, Roberta L Keller3
1Harvard Neonatal-Perinatal Fellowship Program, Boston, MA USA.
Insights
Bronchopulmonary dysplasia (BPD) in preterm infants stems from impaired lung development due to antenatal factors and placental dysfunction. Understanding these mechanisms is key to developing early preventive therapies for BPD.
Area of Science:
- Neonatology
- Pulmonary Medicine
- Developmental Biology
Background:
- Bronchopulmonary dysplasia (BPD) is a significant cause of morbidity and mortality in preterm infants.
- BPD involves arrested lung vascular and alveolar growth, increasing pulmonary hypertension risk.
- Pathogenesis and prevention strategies for BPD remain poorly understood.
Purpose of the Study:
- To explore the impact of antenatal factors on lung development and BPD pathogenesis.
- To investigate the role of placental dysfunction in the development of "new BPD".
- To identify potential targets for early BPD preventive therapies.
Main Methods:
- Review of epidemiologic studies on BPD and preterm birth.
- Analysis of data from animal models investigating antenatal stress and placental function.
- Examination of mechanisms linking placental dysfunction to altered lung development.
Main Results:
- Epidemiologic data indicate "new BPD" is influenced by antenatal factors.
- Placental dysfunction is a key mediator of antenatal stress effects on lung development.
- Animal models support the link between antenatal stress, placental changes, and BPD.
Conclusions:
- Antenatal factors, particularly placental dysfunction, significantly impact lung development and contribute to BPD.
- Further research into these mechanisms may reveal novel preventive strategies for BPD.
- Targeting antenatal interventions holds promise for reducing BPD incidence.
Abstract:
Bronchopulmonary dysplasia (BPD) remains a major cause of late morbidities and death after preterm birth. BPD is characterized by an arrest of vascular and alveolar growth and high risk for pulmonary hypertension; yet mechanisms contributing to its pathogenesis and early strategies to prevent BPD are poorly understood. Strong epidemiologic studies have shown that the "new BPD" reflects the long-lasting impact of antenatal factors on lung development, partly due to placental dysfunction, as reflected in recent data from animal models. Improved understanding of mechanisms through which antenatal stress alters placental function and contributes to BPD may lead to preventive therapies.
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