ADAM17-induced shedding of glypican-1 as a mechanism of impaired endothelial shear stress mechanotransduction

American Journal of Physiology-Cell Physiology 2026 Open access

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Authors: Marc A. Augenreich, Larissa Ferreira-Santos, Gavin Power, Francisco I. Ramirez‐Perez, Juan D. Gonzalez-Vallejo, M. Williams, Natnicha Imkaew, Min Jeong Cho, Andrew A. Wheeler, Camila Manrique-Acevedo, Luis A. Martinez‐Lemus, Jaume Padilla
DOI: 10.1152/ajpcell.00794.2025
Cited by: 3
References: 33

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.

Fields of Study & Subjects

Glycosylation and Glycoproteins Research Erythrocyte Function and Pathophysiology Blood properties and coagulation

Publication details

Journal / source
American Journal of Physiology-Cell Physiology
Publisher
American Physiological Society
Volume
330
Issue
3
Pages
C631–C642
Publication date
16 January 2026
Language
EN