Human Aortic Stenotic Valve-Derived Extracellular Vesicles Induce Endothelial Dysfunction and Thrombogenicity Through AT1R/NADPH Oxidases/SGLT2 Pro-Oxidant Pathway.
SGLT2i
SVD
TAVI
TAVR
aortic stenosis
extracellular vesicles
inflammation
leaflet
microparticles
thrombosis
Journal
JACC. Basic to translational science
ISSN: 2452-302X
Titre abrégé: JACC Basic Transl Sci
Pays: United States
ID NLM: 101677259
Informations de publication
Date de publication:
Jul 2024
Jul 2024
Historique:
received:
10
05
2023
revised:
22
02
2024
accepted:
22
02
2024
medline:
22
8
2024
pubmed:
22
8
2024
entrez:
22
8
2024
Statut:
epublish
Résumé
Pathological tissues release a variety of factors, including extracellular vesicles (EVs) shed by activated or apoptotic cells. EVs trapped within the native pathological valves may act as key mediators of valve thrombosis. Human aortic stenosis EVs promote activation of valvular endothelial cells, leading to endothelial dysfunction, and proadhesive and procoagulant responses.
Identifiants
pubmed: 39170957
doi: 10.1016/j.jacbts.2024.02.012
pii: S2452-302X(24)00090-1
pmc: PMC11334416
doi:
Types de publication
Journal Article
Langues
eng
Pagination
845-864Informations de copyright
© 2024 The Authors.
Déclaration de conflit d'intérêts
This work was supported by an unrestricted research grant by the Groupe pour l’Enseignement de la Recherche Cardio-vasculaire en Alsace, France. The authors have reported that they have no relationships relevant to the contents of this paper to disclose.