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Vascular Endothelial Growth Factor as Molecular Target for Bronchopulmonary Dysplasia Prevention in Very Low Birth
Serafina Perrone1, Sara Manti2, Luca Buttarelli1
1Neonatology Unit, Pietro Barilla Children's Hospital, Department of Medicine and Surgery, University of Parma, Via Gramsci 14, 43126 Parma, Italy.
Insights
Bronchopulmonary dysplasia (BPD) in preterm newborns involves inflammation and oxidative stress. This review highlights the role of vascular endothelial growth factor-A (VEGFA) in BPD pathogenesis.
Area of Science:
- Neonatal Medicine
- Pulmonology
- Developmental Biology
Background:
- Bronchopulmonary dysplasia (BPD) is a significant neonatal care challenge, often defined by treatment rather than clear criteria.
- BPD pathogenesis is multifactorial, linked to prenatal and postnatal risks like IUGR, PDA, sepsis, and mechanical ventilation.
- Inflammation and oxidative stress are key mechanisms underlying BPD development.
Purpose of the Study:
- To review inflammatory pathways implicated in BPD onset in preterm infants.
- To focus on the critical role of vascular endothelial growth factor-A (VEGFA) in BPD.
- To summarize current and emerging evidence on VEGFA and inflammation in BPD.
Main Methods:
- Literature review of experimental models and clinical studies.
- Analysis of inflammatory pathways and oxidative stress in BPD.
- Focus on the function of VEGFA in lung development and disease.
Main Results:
- Prenatal and postnatal factors contribute to distorted lung growth and altered mesenchymal cell function in BPD.
- VEGFA is a key regulator of vascular development, and its dysfunction is implicated in BPD.
- Inflammation and oxidative stress are central to the mechanisms driving BPD.
Conclusions:
- Understanding inflammatory pathways and VEGFA's role is crucial for BPD management.
- Further research into VEGFA and inflammation may lead to novel therapeutic strategies for preterm infants.
- BPD remains a complex condition requiring a comprehensive approach addressing its multifactorial nature.
Abstract:
Bronchopulmonary dysplasia (BPD) still represents an important burden of neonatal care. The definition of the disease is currently undergoing several revisions, and, to date, BPD is actually defined by its treatment rather than diagnostic or clinic criteria. BPD is associated with many prenatal and postnatal risk factors, such as maternal smoking, chorioamnionitis, intrauterine growth restriction (IUGR), patent ductus arteriosus (PDA), parenteral nutrition, sepsis, and mechanical ventilation. Various experimental models have shown how these factors cause distorted alveolar and vascular growth, as well as alterations in the composition and differentiation of the mesenchymal cells of a newborn's lungs, demonstrating a multifactorial pathogenesis of the disease. In addition, inflammation and oxidative stress are the common denominators of the mechanisms that contribute to BPD development. Vascular endothelial growth factor-A (VEGFA) constitutes the most prominent and best studied candidate for vascular development. Animal models have confirmed the important regulatory roles of epithelial-expressed VEGF in lung development and function. This educational review aims to discuss the inflammatory pathways in BPD onset for preterm newborns, focusing on the role of VEGFA and providing a summary of current and emerging evidence.
