ArticleTranslational pediatrics2026
Elucidating shared genes and pathways in programmed cell death with necrotizing enterocolitis: insights into novel therapeutic targets and glutathione.
Article in Translational pediatrics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Necrotizing enterocolitis (NEC) is a severe neonatal intestinal disease with high mortality, and effective pharmacological therapies remain limited. Increasing evidence suggests that multiple forms of programmed cell death are involved in NEC pathogenesis. Glutathione (GSH), has shown potential protective effects against oxidative stress and inflammation injury, but its role and underlying mechanisms in NEC remain unclear. This study aimed to elucidate the shared molecular mechanisms underlying ferroptosis, pyroptosis, necroptosis and autophagy in NEC, and to investigate the protective role and regulatory pathways of GSH against these forms of programmed cell death. Methods: To address these knowledge gaps, we comprehensively analyzed ferroptosis, pyroptosis, necroptosis, and autophagy gene sets from GeneCards and microarray data for NEC, aiming to identify shared differentially expressed genes (DEGs) biomarkers and pathways involved in programmed cell death during NEC pathogenesis. A series of bioinformatics analyses were performed, including Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment analyses, protein-protein interaction (PPI) networks, biological characterization, and transcription factors (TFs)-gene interactions. Key regulators of cell death were further validated in NEC mouse model, Caco-2 experiments, and clinical samples. Additionally, the potential interactions between GSH and hub genes encoded proteins were preliminarily explored by molecular docking. Results: In this study, 11 potential target genes associated with both NEC and cell death were identified by intersecting DEGs. Subsequently, six hub genes ( Conclusions: TLR4, NLRP3 and NFKB1 represent shared molecular mediators of ferroptosis, pyroptosis, necroptosis and autophagy in the pathogenesis of NEC. GSH may alleviate intestinal necrosis in NEC by downregulating the expression of TLR4, NLRP3 and NFKB1.
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