| Autor: |
Fuhr JC; Universidade de Passo Fundo, Instituto de Ciências Biológicas, Passo Fundo, RS, Brazil., Ramos MEK; Universidade de Passo Fundo, Faculdade de Medicina, Passo Fundo, RS, Brazil., Piovesan F; Universidade de Passo Fundo, Faculdade de Medicina, Passo Fundo, RS, Brazil., Renner LO; Universidade de Passo Fundo, Faculdade de Medicina, Passo Fundo, RS, Brazil., Siqueira LO; Universidade de Passo Fundo, Instituto de Ciências Biológicas, Passo Fundo, RS, Brazil. |
| Abstrakt: |
Diabetes mellitus and arterial hypertension are among the five risk factors that increase mortality in the world. Both are chronic, non-communicable diseases (NCDs), that have a pathophysiological association. Advanced glycation end products (AGEs), produced by the lack of glycemic control in diabetic patients, interact with their AGE receptors (AGER) resulting in increased arterial stiffness, inflammation and endothelial changes - which increases the risk of developing hypertension and other complications. We ran a systematic review in Pubmed, SciELO, Cochrane Library and Web of Science databases using keywords and Boolean operators to optimize the search, with the objective of assessing the mechanism of non-enzymatic glycation of proteins present in patients with diabetes and its correlation with the onset of hypertension, exposing all the endothelial and cellular damage caused by AGEs. We found 719 papers, of which 99 were read in full, and 26 met the eligibility criteria and were included in the present review. AGEs should be considered one of the main cardiometabolic risk factors. Reducing the AGE-AGER interaction will result in cardiovascular protection and increased life expectancy. |
