ArticleCommunications biology2022
Macrophage-derived IGF-1 protects the neonatal intestine against necrotizing enterocolitis by promoting microvascular development.
Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Beyond immunity: macrophage plasticity in vascular regeneration.npj biomedical innovations · 2026Review
- Article
- Tissue-resident macrophages maintain choroidal homeostasis by complement dependent and independent mechanisms.Journal of neuroinflammation · 2026Article
- Kupffer cells control neonatal hepatic metabolism via Igf1 signaling.Development (Cambridge, England) · 2026Article
- Development and functional adaptation of intestinal macrophages across the lifespan.Clinical & translational immunology · 2026Review
- Gut-Brain Axis in Preterm Infants with Surgical Necrotizing Enterocolitis.American journal of perinatology · 2025Review
- The Trim32-DPEP2 axis is an inflammatory switch in macrophages during intestinal inflammation.Cell death and differentiation · 2025Article
- Impact of initial postweaning feed intake on weanling piglet metabolism, gut health, and immunity.Journal of animal science · 2025Article
- Neuroprotection of IGF-1 in neonatal hypoxic-ischemic brain injury through downregulation of FoXO3a-PUMA pathway.Frontiers in cellular neuroscience · 2025Article
- Insulin-like growth factor-1 effects on kidney development in preterm piglets.Pediatric research · 2024Article
- Microbiota regulates neonatal disease tolerance to virus-evoked necrotizing enterocolitis by shaping the STAT1-NLRC5 axis in the intestinal epithelium.Cell host & microbe · 2024Article
- Gut microbiota differences in five-year-old children that were born preterm with a history of necrotizing enterocolitis: A pilot trial.iScience · 2024Article
- Recombinant IGF-1/BP3 protects against intestinal injury in a neonatal mouse NEC model.Pediatric research · 2024Article
- Biomaterials for immunomodulation in wound healing.Regenerative biomaterials · 2024Review
- New insights into intestinal macrophages in necrotizing enterocolitis: the multi-functional role and promising therapeutic application.Frontiers in immunology · 2023Review
- State-of-the-art review and update ofFrontiers in pediatrics · 2023Review
- Feeding mode influences dynamic gut microbiota signatures and affects susceptibility to anti-CD3 mAb-induced intestinal injury in neonatal mice.American journal of physiology. Gastrointestinal and liver physiology · 2022Article
- Necrotizing enterocolitis: Bench to bedside approaches and advancing our understanding of disease pathogenesis.Frontiers in pediatrics · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Necrotizing enterocolitis (NEC) is a deadly bowel necrotic disease of premature infants. Low levels of plasma IGF-1 predispose premature infants to NEC. While increasing evidence suggests that defective perinatal intestinal microvascular development plays a role in NEC, the involved mechanism remains incompletely understood. We report here that serum and intestinal IGF-1 are developmentally regulated during the perinatal period in mice and decrease during experimental NEC. Neonatal intestinal macrophages produce IGF-1 and promote endothelial cell sprouting in vitro via IGF-1 signaling. In vivo, in the neonatal intestine, macrophage-derived IGF-1 promotes VEGF expression and endothelial cell proliferation and protects against experimental NEC. Exogenous IGF-1 preserves intestinal microvascular density and protects against experimental NEC. In human NEC tissues, villous endothelial cell proliferation and IGF-1- producing macrophages are decreased compared to controls. Together, our results suggest that defective IGF-1-production by neonatal macrophages impairs neonatal intestinal microvascular development and predisposes the intestine to necrotizing enterocolitis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.