ArticlePediatric research2022
Eliglustat prevents Shiga toxin 2 cytotoxic effects in human renal tubular epithelial cells.
Article in Pediatric research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Shiga toxin delivery in extracellular vesicles induces high mortality and severe kidney injury in a Gb3-dependent manner.PLoS pathogens · 2026Article
- Targeting pH regulation in cancer: combined mild alkaline treatment and NHE1 inhibition as a potential therapy for clear cell renal cell carcinoma.Molecular and cellular biochemistry · 2026Article
- Antibody Screening and Binding Prediction Analysis Targeting Stx2.Antibodies (Basel, Switzerland) · 2026Article
- Eliglustat prevents acute kidney injury caused by Shiga toxin 2 in lethal and sublethal rat models of hemolytic uremic syndrome.Frontiers in pharmacology · 2026Article
- Model-informed repurposing of eliglustat for treatment and prophylaxis of Shiga toxin-producing Escherichia coli hemolytic-uremic syndrome (STEC-HUS) in children.Pediatric nephrology (Berlin, Germany) · 2025Article
- Monocytes serve as Shiga toxin carriers during the development of hemolytic uremic syndrome.Cellular & molecular biology letters · 2025Article
- Neutrophil and neutrophil extracellular traps in acute kidney injury: from mechanisms to treatments.Frontiers in immunology · 2025Review
- Modeling Shiga toxin-induced human renal-specific microvascular injury.Integrative biology : quantitative biosciences from nano to macro · 2024Article
- Article
- Diagnosis and Treatment for Shiga Toxin-ProducingToxins · 2022Review
- EnterohemorrhagicInternational journal of molecular sciences · 2022Review
- Role of Globotriaosylceramide in Physiology and Pathology.Frontiers in molecular biosciences · 2022Review
- The Shiga Toxin Receptor Globotriaosylceramide as Therapeutic Target in Shiga ToxinMicroorganisms · 2021Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundShiga toxin-producing Escherichia coli is responsible for post-diarrheal (D+) hemolytic uremic syndrome (HUS), which is a cause of acute renal failure in children. The glycolipid globotriaosylceramide (Gb3) is the main receptor for Shiga toxin (Stx) in kidney target cells. Eliglustat (EG) is a specific and potent inhibitor of glucosylceramide synthase, first step of glycosphingolipid biosynthesis, actually used for the treatment of Gaucher's disease. The aim of the present work was to evaluate the efficiency of EG in preventing the damage caused by Stx2 in human renal epithelial cells.
methodsHuman renal tubular epithelial cell (HRTEC) primary cultures were pre-treated with different dilutions of EG followed by co-incubation with EG and Stx2 at different times, and cell viability, proliferation, apoptosis, tubulogenesis, and Gb3 expression were assessed.
resultsIn HRTEC, pre-treatments with 50 nmol/L EG for 24 h, or 500 nmol/L EG for 6 h, reduced Gb3 expression and totally prevented the effects of Stx2 on cell viability, proliferation, and apoptosis. EG treatment also allowed the development of tubulogenesis in 3D-HRTEC exposed to Stx2.
conclusionsEG could be a potential therapeutic drug for the prevention of acute kidney injury caused by Stx2. IMPACT: For the first time, we have demonstrated that Eliglustat prevents Shiga toxin 2 cytotoxic effects on human renal epithelia, by reducing the expression of the toxin receptor globotriaosylceramide. The present work also shows that Eliglustat prevents Shiga toxin 2 effects on tubulogenesis of renal epithelial cells. Eliglustat, actually used for the treatment of patients with Gaucher's disease, could be a therapeutic strategy to prevent the renal damage caused by Shiga toxin.
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