Abstract：
Chronic inflammation is a common foundation for the development of many non-communicable diseases, particularly diabetes, atherosclerosis, and tumors. The activation of the axis involving Advanced Glycation End products (AGEs) and their receptor RAGE is a key promotive factor in the chronic inflammation process, influencing the pathological progression of these diseases. The accumulation of AGEs in the body results from an increase in glycation reactions and oxidative stress, especially pronounced in individuals with diabetes. By binding to RAGE, AGEs activate signaling pathways such as NF-κB, promoting the release of inflammatory factors, exacerbating cell damage and inflammation, and further advancing the formation of atherosclerotic plaques and tumor development. This review will delve into the molecular mechanisms by which the AGEs-RAGE axis activates chronic inflammation in the aforementioned diseases, as well as strategies to inhibit the AGEs-RAGE axis, aiming to slow or halt the progression of chronic inflammation and related diseases. This includes the development of AGEs inhibitors, RAGE antagonists, and interventions targeting upstream and downstream signaling pathways. Additionally, the early detection of AGEs levels and RAGE expression as biomarkers provides new avenues for the prevention and treatment of diabetes, atherosclerosis, and tumors.
摘要：
慢性炎症是许多非传染性疾病发展的共同基础，特别是糖尿病，动脉粥样硬化,和肿瘤。涉及晚期糖基化终产物（AGEs）及其受体RAGE的轴的激活是慢性炎症过程中的关键促进因素，影响这些疾病的病理进展。体内AGEs的积累是由于糖化反应和氧化应激的增加，在糖尿病患者中尤其明显。通过绑定到RAGE，AGEs激活信号通路，如NF-κB，促进炎症因子的释放，加剧细胞损伤和炎症，进一步促进动脉粥样硬化斑块的形成和肿瘤的发展。本文就AGEs-RAGE轴激活上述疾病慢性炎症的分子机制进行综述,以及抑制AGEs-RAGE轴的策略，旨在减缓或阻止慢性炎症和相关疾病的进展。这包括AGEs抑制剂的开发，RAGE拮抗剂，以及针对上游和下游信号通路的干预措施。此外,早期检测AGEs水平和RAGE表达作为生物标志物为糖尿病的预防和治疗提供了新的途径。动脉粥样硬化,和肿瘤。
