ArticleCommunications biology2025
L-cystine alleviates necrotizing enterocolitis by regulating ferroptosis and Th17 cell differentiation via the IL-6/STAT3 pathway.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Macrophage metabolic reprogramming via HIF-1α-glycolysis drives osteoblast ferroptosis and bone loss through an IL-6-STAT3-dependent redox axis.Redox report : communications in free radical research · 2026Article
- Elucidating shared genes and pathways in programmed cell death with necrotizing enterocolitis: insights into novel therapeutic targets and glutathione.Translational pediatrics · 2026Article
- Ferroptosis in necrotizing enterocolitis: iron overload-driven intestinal injury and mechanistic insights.Frontiers in pediatrics · 2026Review
- Mechanisms by which tryptophan metabolites enhance intestinal barrier function to prevent necrotizing enterocolitis in preterm infants.Frontiers in immunology · 2026Review
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Authors and funding
6 authors.
Funding
Abstract
Necrotizing enterocolitis (NEC) severely affects preterm infants with limited treatments. Although intestinal homeostasis dysfunction is considered a trigger for NEC, the key targets and mechanisms remain unclear. Using lipopolysaccharide-stimulated colonic epithelial cells and hypothermic hypoxia-induced NEC mice (both sexes), we demonstrate that the gut metabolite L-cystine alleviates intestinal inflammation by balancing Th17/Treg responses and inhibiting ferroptosis. Mechanistically, L-cystine directly targets KIF11 to suppress RC3H1 expression, blocking IL-6 transcripts through transcriptional modifications, thereby inhibiting IL-6 secretion and ferroptosis. Conditioned medium from L-cystine-treated cells inactivates IL-6/STAT3 signaling, reducing pro-inflammatory cytokine release and restoring Th17/Treg balance. Notably, microbiota colonization from NEC preterm infants exacerbates intestinal damage, an effect mitigated by L-cystine and IL-6/STAT3 inhibition. Thus, L-cystine attenuates NEC by suppressing ferroptosis in epithelial cells, restoring immune homeostasis, and preserving intestinal barrier integrity. Targeting intestinal metabolites represents a promising prophylactic and therapeutic strategy for NEC, addressing unmet clinical needs in neonatal intestinal injury management.
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Registered trials
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