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ADAM17 cleaves the insulin receptor ectodomain on endothelial cells and causes vascular insulin resistance

Thaysa Ghiarone, Jorge A. Castorena‐Gonzalez, Christopher Foote, Francisco I. Ramirez‐Perez, Larissa Ferreira‐Santos, Francisco J. Cabral-Amador, Roger de la Torre, Rama Ganga, Andrew A. Wheeler, Camila Manrique‐Acevedo, Jaume Padilla, Luis A. Martinez‐Lemus

2022American Journal of Physiology-Heart and Circulatory Physiology20 citationsDOIOpen Access PDF

Abstract

To our knowledge, this is the first study to investigate the involvement of ADAM17 in causing impaired insulin-induced vasodilation in T2D. We provide evidence that ADAM17 activity is increased in the vasculature of patients with T2D and support the notion that ADAM17-mediated shedding of endothelial IRα ectodomains is a novel mechanism causing vascular insulin resistance. Our results highlight that targeting ADAM17 activity may be a potential therapeutic strategy to correct vascular insulin resistance in T2D.

Topics & Concepts

EctodomainInsulin resistanceInsulinVasodilationInsulin receptorInternal medicineEndocrinologyReceptorMedicineReceptor Mechanisms and SignalingDiabetes Treatment and ManagementHER2/EGFR in Cancer Research
ADAM17 cleaves the insulin receptor ectodomain on endothelial cells and causes vascular insulin resistance | Litcius