ArticleBMC cardiovascular disorders2024
OGT-mediated O-GlcNAcylation regulates macrophage polarization in heart failure via targeting IRF1.
Article in BMC cardiovascular disorders, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Distinct O-Linked Glycosylation Systems in Signaling and Immune Regulation.International journal of molecular sciences · 2026Review
- O-GlcNAcylation of AZGP1 regulates M1/M2 macrophage polarization in diabetic periodontitis.Odontology · 2026Article
- Immune Cell-Mediated Inflammation in Heart Failure: Subset Heterogeneity and Targeted Therapy.International journal of general medicine · 2026Review
- O-GlcNAcylation in diabetic cardiac remodeling and a proposed endothelial-macrophage-fibroblast network.Frontiers in immunology · 2026Review
- Pathogenic glycosyltransferase genes and potential therapeutic drugs in pressure overload-induced heart failure.ESC heart failure · 2025Article
- Hepatic NMNAT1 is required to defend against alcohol-associated fatty liver disease.Science advances · 2025Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
backgroundHeart failure (HF) is a syndrome with complex etiology and high mortality in the world. Macrophage-related inflammation is involved in HF development. O-GlcNAcylation is a post-translational modification that affects pathological processes. This study aimed to investigate the role of O-GlcNAcylation in HF, especially its effect on macrophage polarization.
methodsRaw264.7 cells were treated with lipopolysaccharide (LPS) to induce pro-inflammatory macrophages. HF mice were generated by transverse aortic constriction (TAC). After knockdown of OGT or overexpressing IRF1, macrophage polarization was evaluated using quantitative real-time polymerase chain reaction and flow cytometry. Underlying mechanism was analyzed using bioinformatic analysis, co-immunoprecipitation (co-IP), IP, and western blotting.
resultsThe results showed that O-GlcNAcylation and OGT levels were high in LPS-treated Raw264.7 cells. OGT knockdown inhibited pro-inflammatory macrophage polarization and promoted anti-inflammatory macrophage polarization caused by LPS, and alleviated TAC-induced cardiac dysfunction and fibrosis. Mechanistically, OGT silence suppressed O-GlcNAcylation of IRF1 at Ser (S)283 site. IRF1 overexpression reversed macrophage polarization modulated by OGT knockdown.
conclusionSilencing of OGT promotes macrophage polarization from pro-inflammatory to anti-inflammatory phenotype to alleviate HF through O-GlcNAcylation of IRF1. The findings suggest that O-GlcNAcylation has the potential to treat HF.
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