ArticleApplied biochemistry and biotechnology2026
circGAB1 Activates Autophagy to Promote Sepsis-Associated Acute Kidney Injury by Interacting with ELAVL1 to Activate the HMGB3/β-catenin Signaling Pathway.
Article in Applied biochemistry and biotechnology, 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
Sepsis-associated acute kidney injury (SA-AKI) represents a prevalent complication in critically ill patients, and its molecular mechanisms remain incompletely understood. Circular RNAs (circRNAs) have been increasingly implicated in the pathogenesis of multiple diseases; however, the function and mechanism of circGAB1 in SA-AKI remain largely unknown. Differentially expressed circRNAs in SA-AKI were identified from the Gene Expression Omnibus database (dataset GSE232404), and circGAB1 expression was confirmed by quantitative real-time polymerase chain reaction. Its stability and subcellular localization were assessed using RNase R digestion, actinomycin D assay, and fluorescence in situ hybridization. circGAB1 was knocked down with short hairpin RNA, and its effects on autophagy, cell viability, and apoptosis were evaluated using Cell Counting Kit-8, Western blot, monodansylcadaverine staining, lactate dehydrogenase release, and flow cytometry. Interactions among circGAB1, ELAV-like RNA-binding protein 1 (ELAVL1), and High Mobility Group Box 3 (HMGB3) were examined by RNA pull-down, RNA immunoprecipitation, and dual-luciferase reporter assays. In vivo, adenovirus-mediated knockdown or overexpression was employed to assess the role of the circGAB1/ELAVL1/HMGB3 axis in autophagy, the β-catenin pathway, and renal function. Analysis of the public GEO dataset revealed that circGAB1 was significantly upregulated in SA-AKI samples, and its high expression was also verified in SA-AKI model cells. Additionally, circGAB1 exhibited a nucleocytoplasmic subcellular localization pattern. In SA-AKI mice, knockdown of circGAB1 inhibited autophagy, reduced cellular damage, and improved renal function. Mechanistically, circGAB1 bound to ELAVL1 to enhance HMGB3 mRNA stability, thereby activating the β-catenin pathway and promoting autophagy. Overexpression of ELAVL1 or HMGB3 reversed the suppressive effects of circGAB1 knockdown on autophagy and the β-catenin pathway. circGAB1 enhances HMGB3 mRNA stability by binding to ELAVL1, thereby activating the β-catenin pathway and autophagy to promote SA-AKI. Targeting circGAB1 may provide a new strategy for SA-AKI treatment.
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