Intestinal microcirculation and necrotizing enterocolitis: The vascular endothelial growth factor system

Rakhee M. Bowker, Xiaocai Yan, Isabelle G. De Plaen*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

58 Scopus citations


Necrotizing enterocolitis (NEC), a leading cause of morbidity and mortality in preterm neonates, is a devastating disease characterized by intestinal tissue inflammation and necrosis. NEC pathogenesis is multifactorial but remains unclear. Translocation of bacteria and/or bacterial products across a weak intestinal barrier in the setting of impaired mucosal immunity leads to an exaggerated inflammatory response and secondary mucosal epithelial injury. In addition to prematurity, other risk factors for NEC include congenital heart disease, maternal pre-eclampsia with placental vascular insufficiency, severe anemia and blood transfusion – all conditions that predispose the intestine to ischemia. We recently found that maldevelopment of the intestinal microvasculature plays an important role in NEC pathogenesis. Here we review the evidence supporting a role for defective development of the intestinal mucosal microvasculature and perturbations of intestinal blood flow in NEC, emphasizing the importance of vascular endothelial growth factor (VEGF) and the VEGF receptor-2 signaling pathway.

Original languageEnglish (US)
Pages (from-to)411-415
Number of pages5
JournalSeminars in Fetal and Neonatal Medicine
Issue number6
StatePublished - Dec 2018


  • Angiogenesis
  • Intestinal ischemia
  • Intestinal microvasculature
  • Intrauterine infection
  • Necrotizing enterocolitis
  • Vascular endothelial growth factor
  • Vascular endothelial growth factor receptor 2
  • intrauterine inflammation

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health


Dive into the research topics of 'Intestinal microcirculation and necrotizing enterocolitis: The vascular endothelial growth factor system'. Together they form a unique fingerprint.

Cite this