ArticleAmerican journal of physiology. Cell physiology2026
ADAM17-induced shedding of glypican-1 as a mechanism of impaired endothelial shear stress mechanotransduction.
Article in American journal of physiology. Cell physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Going with the flow: endothelial dysfunction in type 2 diabetes.Function (Oxford, England) · 2026Article
- Endothelial CD44 cleavage by ADAM17 impairs shear stress mechanotransduction.Function (Oxford, England) · 2026Article
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Authors and funding
12 authors.
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Abstract
Endothelial dysfunction occurs early in the pathogenesis of type 2 diabetes (T2D)-associated cardiovascular disease. Previous work has revealed that endothelial glycocalyx mechanosensing structures are degraded in T2D, likely contributing to impaired shear stress mechanotransduction and consequent blunted vasodilation. Evidence from proteomic analysis suggests that glypican-1, a well-known mechanosensor, is a substrate of the proinflammatory enzyme ADAM17. A critical step in ADAM17 activation is externalization of phosphatidylserine (PS) to the outer leaflet of the plasmalemma, which can be enacted by the Ca
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