Selenium deficiency is functionally linked with the molecular etiopathogenesis of necrotizing enterocolitis (NEC)

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dc.contributor.authorGurunluoglu, Kubilay
dc.contributor.authorDundar, Muhammed
dc.contributor.authorUnver, Turgay
dc.contributor.authorTurgut, Hatice
dc.contributor.authorGurunluoglu, Semra
dc.contributor.authorAkpinar, Necmettin
dc.contributor.authorAtes, Hasan
dc.date.accessioned2026-04-04T13:37:30Z
dc.date.available2026-04-04T13:37:30Z
dc.date.issued2025
dc.departmentİnönü Üniversitesi
dc.description.abstractNecrotizing enterocolitis (NEC) is a severe and often catastrophic gastrointestinal emergency that predominantly affects neonates, especially those born prematurely, and is associated with high rates of morbidity and mortality. Despite its significant clinical impact, the precise etiology and molecular pathogenesis of NEC remain incompletely understood. In this study, we conducted global transcriptomic profiling using high-throughput RNA sequencing in 11 premature neonates diagnosed with NEC, following rigorous inclusion and exclusion criteria. Compared to healthy controls, we identified 1,204 differentially expressed genes (DEGs), including 636 upregulated and 568 downregulated transcripts. Notably, genes involved in hypoxia-induced apoptosis (e.g., HIF1 AAS3, HIF1 AAS1), the caspase cascade (BCL2, BCL6, CASP5, CASP7), and inflammation (IL1RAP, IL6ST, TNFAIP3, TNFRSF10 A, TLR6, TLR10) were significantly upregulated. In contrast, IL18, a key modulator of inflammatory responses, was downregulated. Interestingly, several genes encoding selenoproteins (GPX1, GPX4, SELENON, SELENOM, SELENOF, SELENOW, SELENOT) were also downregulated, suggesting molecular evidence of selenium deficiency. Gene ontology and pathway enrichment analyses revealed widespread dysregulation in pathways related to hypoxia response, systemic inflammation, coagulation, antimicrobial defense, mitochondrial function, autophagy, selenium metabolism, and apoptosis. Collectively, our findings provide novel insights into the molecular underpinnings of NEC in premature infants and suggest that systemic hypoxia, oxidative stress, selenium deficiency, and programmed cell death contribute significantly to its pathogenesis.
dc.description.sponsorshipScientific and Technological Research Council of Turkiye (TUBIdot;TAK); Inonu University Scientific Research Project Coordination Unit [TOA-2024-3709]
dc.description.sponsorshipOpen access funding provided by the Scientific and Technological Research Council of Turkiye (TUB & Idot;TAK). This work was sup-ported by Inonu University Scientific Research Project Coordination Unit (project code: TOA-2024-3709).
dc.identifier.doi10.1007/s10142-025-01628-8
dc.identifier.issn1438-793X
dc.identifier.issn1438-7948
dc.identifier.issue1
dc.identifier.orcid0000-0002-8315-1765
dc.identifier.orcid0000-0001-6509-2012
dc.identifier.orcid0000-0003-4722-1188
dc.identifier.orcid0000-0002-9737-859X
dc.identifier.orcid0000-0002-4022-1276
dc.identifier.orcid0000-0001-6760-443X
dc.identifier.orcid0000-0001-5317-7537
dc.identifier.pmid40459789
dc.identifier.scopus2-s2.0-105007795063
dc.identifier.scopusqualityQ3
dc.identifier.urihttps://doi.org/10.1007/s10142-025-01628-8
dc.identifier.urihttps://hdl.handle.net/11616/109875
dc.identifier.volume25
dc.identifier.wosWOS:001502689700001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpringer Heidelberg
dc.relation.ispartofFunctional & Integrative Genomics
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WOS_20250329
dc.subjectHypoxia-induced apoptosis
dc.subjectNecrotizing Enterocolitis
dc.subjectPremature infants
dc.subjectSelenium deficiency
dc.titleSelenium deficiency is functionally linked with the molecular etiopathogenesis of necrotizing enterocolitis (NEC)
dc.typeArticle

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