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

Mirelly Cunha da Silva1, Vanessa Maria Dos Santos1, Matheus Vinícius B da Silva1

  • 1Laboratory of Nutrition, Physical Activity and Phenotypic Plasticity, Federal University of Pernambuco, Vitória de Santo Antão, Brazil.

Frontiers in Molecular Biosciences
|October 31, 2022
PubMed

Insights

Disintegrin and Metalloprotease 17 (ADAM17) impacts hypertension by affecting angiotensin converting enzyme type 2 (ACE2) and nitric oxide (NO) pathways. This overview explores ADAM17

Area of Science:

  • Biochemistry
  • Cardiovascular Physiology
  • Molecular Biology

Background:

  • A Disintegrin and Metalloprotease 17 (ADAM17), also known as tumor necrosis factor-ɑ (TNF-ɑ) convertase (TACE), is a protease regulating growth factors, chemokines, and cytokines.
  • ADAM17 plays a role in hypertension, particularly through the shedding of angiotensin converting enzyme type 2 (ACE2), which impairs angiotensin 1-7 [Ang-(1-7)] production, leading to vasodilation issues, renal damage, and cardiac hypertrophy.

Purpose of the Study:

  • To provide an overview of the role of ADAM17 in the context of nitric oxide (NO) pathways.
  • To elucidate the mechanisms by which ADAM17 influences NO formation and bioavailability.

Main Methods:

  • Literature review focusing on ADAM17, ACE2, Ang-(1-7), Mas receptor (MasR), and nitric oxide (NO) signaling.
  • Analysis of existing studies on the interplay between ADAM17 activity and endothelial function.

Main Results:

  • ADAM17-mediated shedding of ACE2 disrupts the Ang-(1-7)/MasR/NO pathway, contributing to hypertension.
  • Tumor necrosis factor-ɑ (TNF-ɑ), influenced by ADAM17, can decrease NO bioavailability, impairing vasorelaxation.

Conclusions:

  • ADAM17 is a key player in cardiovascular regulation through its influence on NO pathways.
  • Understanding ADAM17's role in NO formation is crucial for developing novel therapeutic strategies for hypertension and related cardiovascular diseases.
Keywords:
endotehliumhypertensioninflammationmetalloproteasenitric oxideoxidative stress

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