ArticleEMBO molecular medicine2022
Inhibition of O-GlcNAcylation protects from Shiga toxin-mediated cell injury and lethality in host.
Article in EMBO molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 14 citations in OpenAlex.
- Cross-talk between glycosylation pathways: Mechanistic insights and implications for human diseases.Molecular metabolism · 2026Review
- Antiproteinuric effect of dapagliflozin attenuates tubule-interstitial injury development in subclinical acute kidney injury animal model.Frontiers in pharmacology · 2026Article
- TargetingbioRxiv : the preprint server for biology · 2025Article
- Advanced Three-Dimensional Cell Culture Models for Investigating EnterohaemorrhagicJournal of microbiology and biotechnology · 2025Review
- Shiga Toxin Type 2 Aggravates G1/S Phase Cell Cycle Arrest, Mediating Caspase-Independent Cell Death under Hyperosmotic Conditions in the Kidney.Journal of microbiology and biotechnology · 2025Article
- Downregulation of O-GlcNAcylation enhances etoposide-induced p53-mediated apoptosis in HepG2 human liver cancer cells.FEBS open bio · 2025Article
- EnterohemorrhagicPathogens (Basel, Switzerland) · 2025Article
- Identification and validation of glycosylation-related gene signatures for prognostic stratification in sepsis.Frontiers in immunology · 2025Article
- Review
- O-GlcNAcylation controls pro-fibrotic transcriptional regulatory signaling in myofibroblasts.Cell death & disease · 2024Article
- ER Stress-Perturbed Intracellular Protein O-GlcNAcylation Aggravates Podocyte Injury in Diabetes Nephropathy.International journal of molecular sciences · 2023Article
- Inhibition of O-GlcNAcylation protects from Shiga toxin-mediated cell injury and lethality in host.EMBO molecular medicine · 2022Article
- Shiga toxin (Stx) type 2-induced increase in O-linked N-acetyl glucosamine protein modification: a new therapeutic target?EMBO molecular medicine · 2022Article
- Intestinal mucus-derived metabolites modulate virulence of a clade 8 enterohemorrhagicFrontiers in cellular and infection microbiology · 2022Article
- Differential effects of glucose and N-acetylglucosamine on genome instability.American journal of cancer research · 2022Article
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Shiga toxins (Stxs) produced by enterohemorrhagic Escherichia coli (EHEC) are the major virulence factors responsible for hemorrhagic colitis, which can lead to life-threatening systemic complications including acute renal failure (hemolytic uremic syndrome) and neuropathy. Here, we report that O-GlcNAcylation, a type of post-translational modification, was acutely increased upon induction of endoplasmic reticulum (ER) stress in host cells by Stxs. Suppression of the abnormal Stx-mediated increase in O-GlcNAcylation effectively inhibited apoptotic and inflammatory responses in Stx-susceptible cells. The protective effect of O-GlcNAc inhibition for Stx-mediated pathogenic responses was also verified using three-dimensional (3D)-cultured spheroids or organoids mimicking the human kidney. Treatment with an O-GlcNAcylation inhibitor remarkably improved the major disease symptoms and survival rate for mice intraperitoneally injected with a lethal dose of Stx. In conclusion, this study elucidates O-GlcNAcylation-dependent pathogenic mechanisms of Stxs and demonstrates that inhibition of aberrant O-GlcNAcylation is a potential approach to treat Stx-mediated diseases.
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