Relationship of advanced glycation end-products in hypertension in diabetic patients: a systematic review

Abstract 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.

摘要：糖尿病与动脉高血压是全球五大致死性危险因素之一。二者均为慢性非传染性疾病（non-communicable diseases, NCDs），且存在病理生理学关联。糖尿病患者因血糖控制不佳产生的晚期糖基化终末产物（Advanced Glycation End Products, AGEs），可与其AGE受体（AGE Receptors, AGER）结合，引发动脉僵硬、炎症反应及内皮细胞改变，进而升高高血压及其他并发症的发病风险。
本研究在PubMed、SciELO、Cochrane Library及Web of Science数据库中，采用关键词与布尔运算符优化检索策略，开展系统综述，旨在评估糖尿病患者体内蛋白质的非酶糖基化机制及其与高血压发病的关联，并阐明晚期糖基化终末产物介导的全部内皮与细胞损伤过程。本次检索共获取719篇文献，其中99篇经全文通读，最终26篇符合纳入标准并被纳入本综述。
晚期糖基化终末产物应被视为主要的心脏代谢危险因素之一。阻断AGEs与AGER的相互作用，可实现心血管保护并延长预期寿命。