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人主动脉狭窄瓣膜来源的细胞外囊泡通过AT1R/烟酰胺腺嘌呤二核苷酸磷酸氧化酶/钠-葡萄糖协同转运蛋白2促氧化途径诱导内皮功能障碍和血栓形成倾向。

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

作者信息

Hmadeh Sandy, Trimaille Antonin, Matsushita Kensuke, Marchandot Benjamin, Carmona Adrien, Zobairi Fatiha, Sato Chisato, Kindo Michel, Hoang Tam Minh, Toti Florence, Zibara Kazem, Hamade Eva, Schini-Kerth Valérie, Kauffenstein Gilles, Morel Olivier

机构信息

UR 3074 Translational Cardiovascular Medicine, CRBS, Strasbourg, France.

Department of Cardiovascular Medicine, Nouvel Hôpital Civil, Strasbourg University Hospital, Strasbourg, France.

出版信息

JACC Basic Transl Sci. 2024 May 29;9(7):845-864. doi: 10.1016/j.jacbts.2024.02.012. eCollection 2024 Jul.

DOI:10.1016/j.jacbts.2024.02.012
PMID:39170957
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11334416/
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.

摘要

病理组织会释放多种因子，包括活化或凋亡细胞所释放的细胞外囊泡（EVs）。滞留于天然病理瓣膜内的EVs可能充当瓣膜血栓形成的关键介质。人主动脉瓣狭窄EVs会促进瓣膜内皮细胞的活化，导致内皮功能障碍以及促黏附和促凝血反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3f9/11334416/8dbe151dcd17/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3f9/11334416/81bb207a646a/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3f9/11334416/b95da74ddbbb/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3f9/11334416/777adb2aa08d/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3f9/11334416/0b806c6fec2d/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3f9/11334416/3fae9fb3f304/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3f9/11334416/e20c8329ac19/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3f9/11334416/4b274a1901d1/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3f9/11334416/a95077d0a793/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3f9/11334416/8dbe151dcd17/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3f9/11334416/81bb207a646a/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3f9/11334416/b95da74ddbbb/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3f9/11334416/777adb2aa08d/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3f9/11334416/0b806c6fec2d/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3f9/11334416/3fae9fb3f304/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3f9/11334416/e20c8329ac19/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3f9/11334416/4b274a1901d1/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3f9/11334416/a95077d0a793/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3f9/11334416/8dbe151dcd17/gr8.jpg

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