Angiotensin-converting enzyme 2 and its potential protective effect upon heart

Melaku, Leta

doi:10.4103/amhs.amhs_44_17

Cited by 1 publication

(2 citation statements)

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“…Hyperstimulation of the renin-angiotensin system (RAS), mainly associated with other cardiovascular risk factors, can induce a cascade of deleterious actions, such as an increase in blood pressure (BP) (Melaku, 2018). Hypertension is a multifactorial disease that results from the junction of genetic and environmental factors that present neuroendocrine, hemodynamic, redox and inflammatory components, which combine with each other to induce functional and structural changes in the cardiovascular system.…”

Section: Introductionmentioning

confidence: 99%

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

Silva

Santos

Silva

et al. 2022

Front. Mol. Biosci.

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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.

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Section: Introductionmentioning

confidence: 99%

“…Furthermore, ADAM17 also cleaves the active extracellular ectodomain of ACE2, releasing a soluble form of this enzyme (Figure 1), whose pathophysiology importance is not fully understood. (Melaku, 2018).…”

Section: Introductionmentioning

confidence: 99%