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Author Spotlight: Enhancing Understanding and Treatment Strategies with the NEC-on-a-Chip Model
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Intestinal microcirculation and necrotizing enterocolitis: The vascular endothelial growth factor system
Rakhee M Bowker1, Xiaocai Yan2, Isabelle G De Plaen3
1Section of Neonatology, Department of Pediatrics, Rush University Medical Center, Chicago, IL, USA.
Seminars in Fetal & Neonatal Medicine
|September 15, 2018
Summary
Necrotizing enterocolitis (NEC) in preterm infants involves intestinal damage due to impaired immunity and bacterial issues. Defective microvasculature development and blood flow, linked to VEGF signaling, are key factors in NEC.
Area of Science:
- Neonatal Medicine
- Gastroenterology
- Vascular Biology
Background:
- Necrotizing enterocolitis (NEC) is a critical gastrointestinal disease in preterm neonates, causing significant morbidity and mortality.
- Its pathogenesis is complex, involving bacterial translocation, impaired mucosal immunity, and intestinal ischemia.
- Risk factors include prematurity, congenital heart disease, and conditions leading to reduced intestinal blood flow.
Purpose of the Study:
- To review evidence linking defective intestinal microvasculature development to NEC.
- To highlight the role of vascular endothelial growth factor (VEGF) and its signaling pathways in NEC pathogenesis.
Main Methods:
- Review of existing scientific literature and research findings on NEC.
- Analysis of studies focusing on intestinal microvasculature, blood flow, and VEGF signaling in neonates.
Main Results:
- Maldevelopment of the intestinal microvasculature is identified as a significant factor in NEC.
- Perturbations in intestinal blood flow and impaired VEGF signaling contribute to NEC development.
Conclusions:
- Defective development of the intestinal mucosal microvasculature is crucial in NEC.
- Targeting VEGF and its receptor-2 pathway may offer therapeutic strategies for preventing or treating NEC.
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