{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Bowen EE"],"funding":["Kidney Research UK","Medical Research Council","National Institute for Health Research (NIHR)"],"pagination":["761-777.e8"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7617617"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["4(11)"],"pubmed_abstract":["<h4>Background</h4>Shiga 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.<h4>Methods</h4>Transgenic 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.<h4>Findings</h4>Stx-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 endo"],"journal":["Med (New York, N.Y.)"],"pubmed_title":["Shiga toxin targets the podocyte causing hemolytic uremic syndrome through endothelial complement activation."],"pmcid":["PMC7617617"],"funding_grant_id":["MR/K010492/1","MR/T002263/1","MR/W019582/1","G0501901","G0800200","MR/W024187/1","SP/FSGS1/2013","CL-2018-25-002","ACF-2012-25-005","IN_004_20190305","INT_002_20220705","ST_008_20181123","MR/M018237/1","G0901987","TF_007_20151127","RP42/2012"],"pubmed_authors":["Lay AC","Morgan BP","Diatlov D","Satchell SC","Wells S","Bohorquez-Hernandez A","Butler MJ","Wherlock MD","Stewart M","Larkai EMS","Rostam-Shirazi N","Moppett J","Coward RJM","Hurcombe JA","Pope RJP","Welsh GI","Teboul L","Keir LS","Farmer LK","Walker PD","Barrington F","Bruno V","Saleem MA","Ortiz-Sandoval CG","Bowen EE","Licht C"],"additional_accession":[]},"is_claimable":false,"name":"Shiga toxin targets the podocyte causing hemolytic uremic syndrome through endothelial complement activation.","description":"<h4>Background</h4>Shiga 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.<h4>Methods</h4>Transgenic 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.<h4>Findings</h4>Stx-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 endo","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Nov","modification":"2026-06-02T17:34:18.115Z","creation":"2025-07-12T03:04:36.257Z"},"accession":"S-EPMC7617617","cross_references":{"pubmed":["37863058"],"doi":["10.1016/j.medj.2023.09.002"]}}