{"id":"14a6416f9a26","type":"article","url":"https://hartvaat.nl/2026/01/22/heat-shock-eiwitten-70-als-modificatoren-van-endotheelfunctie-bij-de-ziekte-van-/","title":"Heat shock-eiwitten 70 als modificatoren van endotheelfunctie bij de ziekte van Fabry","title_en":"Heat shock protein 70s are modifiers of endothelial function in Fabry disease","category":"chronische nierziekte","category_label":"Nierziekte","professions":["cardioloog","internist"],"tags":[],"journal":"Kidney International","doi":"https://www.kidney-international.org/article/S0085-2538(26)00013-X/fulltext","source_url":"https://doi.org/https://www.kidney-international.org/article/S0085-2538(26)00013-X/fulltext","authors":["Rakesh Verma","Audrey Cleuren","Vania Hinkovska-Galcheva","Ilka Decker","Robert Kelly","David Ginsburg","James A. Shayman"],"significance":5,"published":"2026-01-22","source_date":"2026-01-22","image":"","kennis":["https://hartvaat.nl/kennis/nierziekte/cardiorenal-syndroom/","https://hartvaat.nl/kennis/cardiometabool/diabetes-type-1-en-hart/"],"congress":"","summary_en":"This research identifies heat shock protein 70 family members as disease modifiers of endothelial function in Fabry disease, helping explain the variable clinical phenotypes observed among patients with identical GLA gene mutations.","created":"2026-07-03T10:25:31Z","updated":"2026-07-03T13:24:55Z","licence":"Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.","body_markdown":"De ziekte van Fabry is een systeemaandoening met hart-, vaatziekten en nierziekte. Identieke GLA-genmutaties tonen variabele fenotypen. Dit onderzoek identificeert heat shock-eiwitten 70 als ziektemodificatoren die de endotheelfunctie beïnvloeden.","abstract_original":"Fabry disease (FD) is a systemic disorder with manifestations of heart, vascular, and kidney disease. Identical genetic variants in the α-galactosidase A (GLA) gene exhibit variable clinical phenotypes consistent with the existence of disease modifiers. Prior work in the Gla null mouse identified the vascular endothelium as a primary site for dysfunction associated with FD vasculopathy."}