ReviewFrontiers in immunology2023
New insights into intestinal macrophages in necrotizing enterocolitis: the multi-functional role and promising therapeutic application.
Review in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Identification of diagnostic biomarkers for neonatal necrotizing enterocolitis via machine learning screening and single-cell virtual gene knockout validation.Journal of cell communication and signaling · 2026Article
- Development and functional adaptation of intestinal macrophages across the lifespan.Clinical & translational immunology · 2026Review
- Multi-strain Probiotics for Treatment of Necrotizing Enterocolitis in Preterm Rats: Histological and Immunohistochemical Evaluation.Probiotics and antimicrobial proteins · 2026Article
- Ferroptosis in necrotizing enterocolitis: iron overload-driven intestinal injury and mechanistic insights.Frontiers in pediatrics · 2026Review
- The role of myeloid cells in the pathogenesis of necrotizing enterocolitis; a scoping review.Frontiers in pediatrics · 2026Review
- The BHMT2/MAT1A/AHSG axis promotes M1 macrophage activation and exacerbates necrotizing enterocolitis.Scientific reports · 2025Article
- Targeting TREM1 Ameliorates Necrotizing Enterocolitis in Neonatal Mice by Inhibiting Endoplasmic Reticulum Stress and Regulating Macrophage Polarization.Digestive diseases and sciences · 2025Article
- Spinal Cord Injury 2.0: Bridging the Gap Between Neurobiology, Technology, and Hope in the Era of Precision Medicine.Stem cell reviews and reports · 2025Review
- Inhibition of ferroptosis in inflammatory macrophages alleviates intestinal injury in neonatal necrotizing enterocolitis.Cell death discovery · 2025Article
- Human milk extracellular vesicles modulate inflammation and cell survival in intestinal and immune cells.Pediatric research · 2025Article
- Itaconate suppresses neonatal intestinal inflammation via metabolic reprogramming of M1 macrophage.Clinical and translational medicine · 2025Article
- M2-type macrophage nanovesicles regulate the inflammatory response after necrotizing enterocolitis by inducing M1 to M2-like macrophage polarization.Frontiers in cellular and infection microbiology · 2025Article
- Deciphering immune cell interaction aberrations in necrotizing enterocolitis: the regulatory role of DHRS7.Frontiers in immunology · 2025Article
- Umbilical cord mesenchymal stem cell exosomes alleviate necrotizing enterocolitis in neonatal mice by regulating intestinal epithelial cells autophagy.World journal of stem cells · 2024Article
- [Research progress on the relationship between anemia and neonatal necrotizing enterocolitis].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Necrotizing enterocolitis (NEC) is an inflammatory intestinal disease that profoundly affects preterm infants. Currently, the pathogenesis of NEC remains controversial, resulting in limited treatment strategies. The preterm infants are thought to be susceptible to gut inflammatory disorders because of their immature immune system. In early life, intestinal macrophages (IMφs), crucial components of innate immunity, demonstrate functional plasticity and diversity in intestinal development, resistance to pathogens, maintenance of the intestinal barrier, and regulation of gut microbiota. When the stimulations of environmental, dietary, and bacterial factors interrupt the homeostatic processes of IMφs, they will lead to intestinal disease, such as NEC. This review focuses on the IMφs related pathogenesis in NEC, discusses the multi-functional roles and relevant molecular mechanisms of IMφs in preterm infants, and explores promising therapeutic application for NEC.
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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.