A naukri.com initiative
Bioengineer
1w
382
Image Credit: Bioengineer
Semaphorin Loss and Reduced FOXF1 Link BPD, PH
- A study in Nature Communications reveals how disruptions in semaphorin signaling pathways and reduced FOXF1 expression contribute to bronchopulmonary dysplasia (BPD) with pulmonary hypertension (PH) in premature infants, offering potential for targeted therapies.
- BPD, a chronic lung disease in preterm infants requiring extended oxygen therapy, poses clinical challenges, especially when complicated by PH, which leads to increased pulmonary artery pressure and higher morbidity and mortality rates.
- Researchers found that loss of semaphorin signaling is linked to impaired lung vascularization and remodeling, key features of BPD with PH, establishing a connection between semaphorin pathways and vascular pathology in neonatal lungs.
- FOXF1, a transcription factor crucial for lung development, is functionally decreased in BPD with PH, exacerbating vascular dysfunction and contributing to vascular rarefaction and elevated pulmonary pressures in affected infants.
- The study shows that semaphorin signaling loss leads to transcriptional repression of FOXF1, disrupting genetic programs necessary for endothelial cell survival and proliferation, resulting in hypoxia-induced vascular remodeling in neonatal pulmonary hypertension.
- The research demonstrates the interdependence of semaphorin pathways and FOXF1 expression, defining a novel pathogenic cascade in lung injury, and identifies downstream targets and interacting partners of FOXF1 that play roles in lung tissue architecture.
- Modulating semaphorin signaling or FOXF1 expression in experimental models partially reversed vascular defects and improved pulmonary pressures, suggesting therapeutic interventions to mitigate BPD with PH and enhance long-term respiratory outcomes in preterm birth survivors.
- This work bridges developmental biology, vascular physiology, and molecular genetics to unravel neonatal lung disease complexities, providing insights for potential biomolecular targets and avenues for drug development to prevent or ameliorate early lung injury.
- The study's findings may lead to biomarker identification for disease severity assessment and individualized therapeutic strategies, prompting a shift towards early interventions in neonatal intensive care.
- Understanding the interplay between genetic predisposition, environmental factors, and semaphorin-FOXF1 signaling modulation is crucial for comprehensive prevention measures and translational research to develop targeted therapies for BPD with PH.
- In summary, the research underscores the significance of semaphorin signaling loss and reduced FOXF1 expression in linking BPD with PH, offering new insights for diagnosis and treatment in the realm of neonatal lung diseases.
Read Full Article
23 Likes
For uninterrupted reading, download the app