ArticleMed (New York, N.Y.)2023
Shiga toxin targets the podocyte causing hemolytic uremic syndrome through endothelial complement activation.
Article in Med (New York, N.Y.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 11 citations in OpenAlex.
- Ribosome-inactivating proteins in bacteria.Microbial genomics · 2026Review
- Shiga toxin delivery in extracellular vesicles induces high mortality and severe kidney injury in a Gb3-dependent manner.PLoS pathogens · 2026Article
- Endothelial-erythrocyte glycocalyx exchange enables liquid biopsies of endothelial function.Nature communications · 2026Article
- RTX-family toxin EhxA drives morphological remodeling and thrombogenesis in RBCs during enterohemorrhagicScience advances · 2026Article
- Antibody Screening and Binding Prediction Analysis Targeting Stx2.Antibodies (Basel, Switzerland) · 2026Article
- A Portable Extended-Gate FET Integrated Sensing System with Low-Noise Current Readout for On-Site Detection ofMicromachines · 2026Article
- Redefining Shiga toxin-induced human cell death as NLRP1- and gasdermin E-mediated pyroptosis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Neutrophil and neutrophil extracellular traps in acute kidney injury: from mechanisms to treatments.Frontiers in immunology · 2025Review
- Weibel-Palade bodies: function and role in thrombotic thrombocytopenic purpura and in diarrhea phase of STEC-hemolytic uremic syndrome.Pediatric nephrology (Berlin, Germany) · 2025Review
- Outcomes from the International Society of Nephrology Hemolytic Uremic Syndromes International Forum.Kidney international · 2024Article
- Gene Therapy for Glomerular Disease.Journal of the American Society of Nephrology : JASN · 2024Article
Corrections and comments
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Authors and funding
26 authors at 8 institutions in 3 countries.
Funding
Abstract
backgroundShiga toxin (Stx)-producing Escherichia coli hemolytic uremic syndrome (STEC-HUS) is the leading cause of acute kidney injury in children, with an associated mortality of up to 5%. The mechanisms underlying STEC-HUS and why the glomerular microvasculature is so susceptible to injury following systemic Stx infection are unclear.
methodsTransgenic mice were engineered to express the Stx receptor (Gb3) exclusively in their kidney podocytes (Pod-Gb3) and challenged with systemic Stx. Human glomerular cell models and kidney biopsies from patients with STEC-HUS were also studied.
findingsStx-challenged Pod-Gb3 mice developed STEC-HUS. This was mediated by a reduction in podocyte vascular endothelial growth factor A (VEGF-A), which led to loss of glomerular endothelial cell (GEnC) glycocalyx, a reduction in GEnC inhibitory complement factor H binding, and local activation of the complement pathway. Early therapeutic inhibition of the terminal complement pathway with a C5 inhibitor rescued this podocyte-driven, Stx-induced HUS phenotype.
conclusionsThis study potentially explains why systemic Stx exposure targets the glomerulus and supports the early use of terminal complement pathway inhibition in this devastating disease.
fundingThis work was supported by the UK Medical Research Council (MRC) (grant nos. G0901987 and MR/K010492/1) and Kidney Research UK (grant nos. TF_007_20151127, RP42/2012, and SP/FSGS1/2013). The Mary Lyon Center is part of the MRC Harwell Institute and is funded by the MRC (A410).
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