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Diabetes and hypertension: Pivotal involvement of purinergic signaling

Authors
  • Reichert, Karine Paula1
  • Castro, Milagros Fanny Vera1
  • Assmann, Charles Elias1
  • Bottari, Nathieli Bianchin1
  • Miron, Vanessa Valéria1
  • Cardoso, Andréia2
  • Stefanello, Naiara1
  • Morsch, Vera Maria Melchiors1
  • Schetinger, Maria Rosa Chitolina1
  • 1 Department of Biochemistry and Molecular Biology, Post-Graduation Program of Biological Sciences: Toxicological Biochemistry, CCNE, Federal University of Santa Maria, Santa Maria, RS, Brazil
  • 2 Academic Coordination, Medicine, Campus Chapecó, Federal University of Fronteira Sul, Chapecó, SC, Brazil
Type
Published Article
Journal
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
Publication Date
Jan 30, 2021
Volume
137
Pages
111273–111273
Identifiers
DOI: 10.1016/j.biopha.2021.111273
PMID: 33524787
PMCID: PMC7846467
Source
PubMed Central
Keywords
Disciplines
  • Review
License
Unknown

Abstract

Diabetes mellitus (DM) and hypertension are highly prevalent worldwide health problems and frequently associated with severe clinical complications, such as diabetic cardiomyopathy, nephropathy, retinopathy, neuropathy, stroke, and cardiac arrhythmia, among others. Despite all existing research results and reasonable speculations, knowledge about the role of purinergic system in individuals with DM and hypertension remains restricted. Purinergic signaling accounts for a complex network of receptors and extracellular enzymes responsible for the recognition and degradation of extracellular nucleotides and adenosine. The main components of this system that will be presented in this review are: P1 and P2 receptors and the enzymatic cascade composed by CD39 (NTPDase; with ATP and ADP as a substrate), CD73 (5′-nucleotidase; with AMP as a substrate), and adenosine deaminase (ADA; with adenosine as a substrate). The purinergic system has recently emerged as a central player in several physiopathological conditions, particularly those linked to inflammatory responses such as diabetes and hypertension. Therefore, the present review focuses on changes in both purinergic P1 and P2 receptor expression as well as the activities of CD39, CD73, and ADA in diabetes and hypertension conditions. It can be postulated that the manipulation of the purinergic axis at different levels can prevent or exacerbate the insurgency and evolution of diabetes and hypertension working as a compensatory mechanism.

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