Endothelial CD44 cleavage by ADAM17 impairs shear stress mechanotransduction

Function 2026 Open access

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Authors: Gavin Power, Min Jeong Cho, Jesús H. Beltrán-Ornelas, Marc A. Augenreich, Natnicha Imkaew, Olubodun Michael Lateef, Francisco Ramírez-Pérez, Larissa Ferreira-Santos, Camila Manrique-Acevedo, Luis A. Martinez-Lemus, Jaume Padilla
DOI: 10.1152/function.113.2025
Cited by: 4
References: 40

Abstract

Impaired flow-mediated dilation (FMD) is an indicator of endothelial dysfunction in type 2 diabetes (T2D). However, the exact cellular and molecular mechanisms contributing to impaired mechanotransduction of shear stress in T2D are incompletely understood. This work supports the novel concept that increased endothelial activity of a disintegrin and metalloproteinase 17 (ADAM17) causes cleavage of cell-surface CD44, leading to loss of hyaluronan (HA)-associated shear stress mechanotransduction.

Fields of Study & Subjects

Proteoglycans and glycosaminoglycans research Blood properties and coagulation Angiogenesis and VEGF in Cancer

Publication details

Journal / source
Function
Publisher
American Physiological Society
Volume
7
Issue
3
Pages
e1132025–e1132025
Publication date
23 March 2026
Language
EN