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Human Aortic Stenotic Valve-Derived Extracellular Vesicles Induce Endothelial Dysfunction and Thrombogenicity Through AT1R/NADPH Oxidases/SGLT2 Pro-Oxidant Pathway.


ABSTRACT: 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.

SUBMITTER: Hmadeh S 

PROVIDER: S-EPMC11334416 | biostudies-literature | 2024 Jul

REPOSITORIES: biostudies-literature

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Human Aortic Stenotic Valve-Derived Extracellular Vesicles Induce Endothelial Dysfunction and Thrombogenicity Through AT1R/NADPH Oxidases/SGLT2 Pro-Oxidant Pathway.

Hmadeh Sandy S   Trimaille Antonin A   Matsushita Kensuke K   Marchandot Benjamin B   Carmona Adrien A   Zobairi Fatiha F   Sato Chisato C   Kindo Michel M   Hoang Tam Minh TM   Toti Florence F   Zibara Kazem K   Hamade Eva E   Schini-Kerth Valérie V   Kauffenstein Gilles G   Morel Olivier O  

JACC. Basic to translational science 20240529 7


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. ...[more]

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