ADAM17-Mediated Shedding of Inflammatory Cytokines in Hypertension

The increase of Angiontesin-II (Ang-II), one of the key peptides of the renin-angiotensin system (RAS), and its binding to the Ang-II type 1 receptor (AT R) during hypertension is a crucial mechanism leading to AD\AM17 activation. Among the reported membrane anchored proteins cleaved by ADAM17, immu...

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Published inFrontiers in pharmacology Vol. 11; p. 1154
Main Authors de Queiroz, Thyago M, Lakkappa, Navya, Lazartigues, Eric
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 29.07.2020
Subjects
brain
inflammation
metalloprotease
periphery
Pharmacology
renin-angiotensin system
metalloprotease
brain
inflammation
periphery
renin-angiotensin system
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Summary:The increase of Angiontesin-II (Ang-II), one of the key peptides of the renin-angiotensin system (RAS), and its binding to the Ang-II type 1 receptor (AT R) during hypertension is a crucial mechanism leading to AD\AM17 activation. Among the reported membrane anchored proteins cleaved by ADAM17, immunological cytokines (TNF-α, IFN-γ, TGF-β, IL-4, IL-10, IL-13, IL-6, FKN) are the major class of substrates, modulation of which triggers inflammation. The rise in ADAM17 levels has both central and peripheral implications in inflammation-mediated hypertension. This narrative review provides an overview of the role of ADAM17, with a special focus on its cellular regulation on neuronal and peripheral inflammation-mediated hypertension. Finally, it highlights the importance of ADAM17 with regards to the biology of inflammatory cytokines and their roles in hypertension.
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Edited by: Robson Augusto Souza Santos, Federal University of Minas Gerais, Brazil
These authors have contributed equally to this work
Reviewed by: Sergey V. Ryzhov, Maine Medical Center, United States; Rodrigo Araujo Fraga-Silva, École Polytechnique Fédérale de Lausanne, Switzerland
This article was submitted to Inflammation Pharmacology, a section of the journal Frontiers in Pharmacology
ISSN:1663-9812
1663-9812
DOI:10.3389/fphar.2020.01154