ArticleRedox report : communications in free radical research2024
Sodium formate induces development-dependent intestinal epithelial injury via necroptosis and apoptosis.
Article in Redox report : communications in free radical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed.
- Necrotizing enterocolitis is exacerbated through SUCNR1/HIF-1α/BNIP3 axis-mediated succinate-induced intestinal epithelial cell apoptosis.Pediatric research · 2026Article
- Deciphering the mechanistic involvement of PANoptosis in FC-MDD comorbidity through the gut-brain axis.Frontiers in immunology · 2026Review
- Identification of potential necroinflammation-associated necroptosis-related biomarkers in necrotizing enterocolitis based on bioinformatics analysis and machine learning.Translational pediatrics · 2025Article
- Sodium formate-induced mitochondrial impairment and cytotoxicity in neuronal cells reveal crucial pathogenic mechanisms underlying diabetic neuropathy and retinopathy.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesNecrotizing enterocolitis (NEC) is a common and sometimes fatal disease affecting premature infants. Elevated formate has been found in the stool of patients with NEC. Sodium formate (NaF) is used to explore the role of formate in the intestinal epithelial injury.
methodsIn this study, 150 mM NaF solution was intraluminally injected in 14-day-old and 28-day-old mice. Mice were sacrificed after 24 h of feces collection, and the blood and small intestinal tissues were collected to detect the pathological damage of intestinal tissue, intestinal permeability, oxidative stress indicators including SOD, HO-1, MDA, and 4-HNE, inflammatory cytokines including IL-1β, TNF-α and IL-6, mitochondrial function such as ATP and PGC-1α in mice intestinal tissue, indicators of the cell death modes including necroptosis-related protein RIPK1 and p-MLKL, and apoptosis- related protein cleaved-caspase-3 and p-AKT (S473).
resultsNaF treatment significantly damaged intestinal epithelial tissue and barrier function, caused mitochondrial dysfunction, manifesting as decreased ATP and PGC-1α levels, increased lipid peroxidation products MDA and 4-HNE, depleted antioxidant enzyme SOD, and upregulated the expression of HO-1. Furthermore, NaF treatment induced inflammatory responses by promoting the release of IL-1β, IL-6 and TNF-α in a development-dependent manner, eventually inducing necroptosis and apoptosis.
conclusionsFormate may be a source of metabolic intestinal injury contributing to the pathogenesis of NEC in human newborns.
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