{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gustafson D"],"funding":["Canadian Cancer Society","Canadian Vascular Network","Canadian Institutes of Health Research","CIHR"],"pagination":["1138-1154"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11058313"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["67(6)"],"pubmed_abstract":["<h4>Aims/hypothesis</h4>A hallmark chronic complication of type 2 diabetes mellitus is vascular hyperpermeability, which encompasses dysfunction of the cerebrovascular endothelium and the subsequent development of associated cognitive impairment. The present study tested the hypothesis that during type 2 diabetes circulating small extracellular vesicles (sEVs) exhibit phenotypic changes that facilitate pathogenic disruption of the vascular barrier.<h4>Methods</h4>sEVs isolated from the plasma of a mouse model of type 2 diabetes and from diabetic human individuals were characterised for their ability to disrupt the endothelial cell (EC) barrier. The contents of sEVs and their effect on recipient ECs were assessed by proteomics and identified pathways were functionally interrogated with smal"],"journal":["Diabetologia"],"pubmed_title":["Circulating small extracellular vesicles mediate vascular hyperpermeability in diabetes."],"pmcid":["PMC11058313"],"funding_grant_id":["PJT148487","PJT173489","702835"],"pubmed_authors":["DiStefano PV","Li RK","Syonov M","Fitzpatrick J","Galant N","Fish JE","Lee WL","Parekh RS","Wang XF","Rathnakumar K","Monnier PP","Boudreau E","Ching C","Gustafson D","Ghaffari S","Wu R","Alibhai F","Husain M","Lau C"],"additional_accession":[]},"is_claimable":false,"name":"Circulating small extracellular vesicles mediate vascular hyperpermeability in diabetes.","description":"<h4>Aims/hypothesis</h4>A hallmark chronic complication of type 2 diabetes mellitus is vascular hyperpermeability, which encompasses dysfunction of the cerebrovascular endothelium and the subsequent development of associated cognitive impairment. The present study tested the hypothesis that during type 2 diabetes circulating small extracellular vesicles (sEVs) exhibit phenotypic changes that facilitate pathogenic disruption of the vascular barrier.<h4>Methods</h4>sEVs isolated from the plasma of a mouse model of type 2 diabetes and from diabetic human individuals were characterised for their ability to disrupt the endothelial cell (EC) barrier. The contents of sEVs and their effect on recipient ECs were assessed by proteomics and identified pathways were functionally interrogated with smal","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jun","modification":"2026-06-02T22:47:51.804Z","creation":"2026-04-21T03:13:46.157Z"},"accession":"S-EPMC11058313","cross_references":{"pubmed":["38489029"],"doi":["10.1007/s00125-024-06120-9"]}}