GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE306nnn/GSE306144/primaryOK200TranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE306144GEOGSEfalseInhibition of APE1 Redox Function Reduces Acute Radiation Enteritis by Blocking JAK-STAT3-Mediated Inflammation and Myeloid Cells RecruitmentAcute radiation enteritis (ARE) is a common serious complication in patients with pelvic and abdominal tumors receiving radiotherapy, for which there is a lack of early specific intervention strategies. The clinical treatment for ARE primarily focuses on symptomatic therapy, lacking effective preventive and intervention measures. This study investigated the bifunctional protein Apurinic/apyrimidinic endonuclease 1/Redox factor 1 (APE1/Ref-1) in ARE pathogenesis. Using tamoxifen-inducible Apex1 knockout mice (Apex1flox/floxCre-ER+), we demonstrate stage-specific functions: APE1 mediates early-phase inflammatory factor release and is indispensable for late-phase myeloid cell infiltration. Crucially, both genetic ablation of APE1 redox function, C64S mutant mice, and pharmacological inhibition via pre-radiation intraperitoneal E3330 administration significantly reduced ARE severity. Mechanistically, APE1 activates the JAK-STAT3 pathway to orchestrate initial cytokine storms and subsequently potentiates neutrophil and macrophage recruitment.Mechanistically, APE1 activates the JAK-STAT3 pathway to orchestrate initial cytokine storms and subsequently potentiates neutrophil and macrophage recruitment. These studies provide new approaches for the prevention of ARE.2026/08/22GSE306144GSM9194029GSM9194034GSM9194033GSM9194030GSM9194032GSM919403134290306144Mus musculus