ArticleScientific reports2025
OGT-mediated O-GlcNAc of FOXO1 promotes the progression of neonatal heart failure via regulating pyroptosis.
Article in Scientific reports, 2025. 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
Neonatal heart failure (HF) is a progressive disease caused by cardiovascular and non-cardiovascular abnormalities. O-linked beta-N-acetylglucosamine (O-GlcNAc), a dynamic post-translational modification, is rapidly cycled on and off proteins by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA), respectively. This study aimed to investigate the role of O-GlcNAc in neonatal HF and the underlying mechanism. Twenty-eight neonatal HF patients and 22 healthy control volunteers were included. In vivo and in vitro HF models were established. Western blotting and RT-qPCR were used to detect the expression of O-GlcNAc, OGT, OGA, and pyroptosis-related indicators. CCK-8 was used to detect the cell viability. Lactate dehydrogenase and propidium iodide staining commercial kits were used to assess the cytotoxicity and apoptosis. The concentrations of interleukin (IL)-1β and IL-18 were analyzed by ELISA. Co-immunoprecipitation was performed to verify the interaction between OGT and forkhead box O1 (FOXO1). Results showed that OGT-mediated O-GlcNAc was elevated in HF. Besides, OGT deficiency suppressed pyroptosis in Angiotensin (Ang)II-treated H9c2 cells. Mechanically, OGT regulated the O-GlcNAc of FOXO1 at S41 site in H9c2 cells. Subsequent rescue experiments indicated that FOXO1 overexpression promoted pyroptosis in AngII-treated H9c2 cells. Final animal studies illustrated that OGT inhibition alleviated myocardial tissue necrosis, myocardial fibrosis, and pathological cardiac dysfunction. In conclusion, OGT-mediated O-GlcNAc of FOXO1 promoted the progression of neonatal HF via regulating pyroptosis, which might provide a new insight for neonatal HF treatment.
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