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Involvement of shedding induced by ADAM17 on the nitric oxide pathway in hypertension

2022; Frontiers Media; Volume: 9; Linguagem: Inglês

10.3389/fmolb.2022.1032177

2296-889X

MAYRA SOCORRO DE OLIVEIRA SILVA, Vanessa Maria dos Santos, Matheus Vinicius Barbosa da Silva, Tereza Cristina Monteiro Melo Prazeres, Maria do Socorro Sousa Cartágenes, Natália Tabosa Machado Calzerra, Thyago Moreira de Queiroz,

Neuropeptides and Animal Physiology

A Disintegrin and Metalloprotease 17 (ADAM17), also called tumor necrosis factor-ɑ (TNF-ɑ) convertase (TACE), is a well-known protease involved in the sheddase of growth factors, chemokines and cytokines. ADAM17 is also enrolled in hypertension, especially by shedding of angiotensin converting enzyme type 2 (ACE2) leading to impairment of angiotensin 1–7 [Ang-(1–7)] production and injury in vasodilation, induction of renal damage and cardiac hypertrophy. Activation of Mas receptor (MasR) by binding of Ang-(1–7) induces an increase in the nitric oxide (NO) gaseous molecule, which is an essential factor of vascular homeostasis and blood pressure control. On the other hand, TNF-ɑ has demonstrated to stimulate a decrease in nitric oxide bioavailability, triggering a disrupt in endothelium-dependent vasorelaxation. In spite of the previous studies, little knowledge is available about the involvement of the metalloprotease 17 and the NO pathways. Here we will provide an overview of the role of ADAM17 and Its mechanisms implicated with the NO formation.