ADAM17-induced shedding of glypican-1 as a mechanism of impaired endothelial shear stress mechanotransduction
Year: 2026
Type: article
Abstract: We provide evidence that neuraminidase, which is elevated in plasma from males and females with type 2 diabetes (T2D), is involved in the activation of endothelial ADAM17 and shedding of the mechanosensor glypican-1. We also provide evidence that neuraminidase-induced ADAM17 activation and consequent glypican-1 shedding are mediated by ANO6 scramblase externalization of phosphatidylserine. Together, this work suggests the neuraminidase-ANO6-ADAM17 axis may be a mechanism underlying impaired endothelial shear stress mechanotransduction in T2D.
Language: English
Subfield: Cell Biology
Domain: Life Sciences
Open Access status: hybrid
Awards: Restoring vasodilator actions of insulin in patients with type 2 diabetes, Development of Novel Tools to Study Mechanisms of Endothelial Insulin Resistance and Dysfunction in Obesity and Diabetes, The HIF2alpha-neuraminidase axis as a mechanism of endothelial dysfunction, Role of neuraminidase activity on endothelial dysfunction in type 2 diabetes, G876207116, ADAM17 mediated cleavage of CD44 impairs mechanotransduction of shear stress, G9000042004, G9000113953
OpenAlex ID: W7124434964