Advanced glycation end-products (AGEs) have been implicated in chronic hyperglycemia and age-related diseases. Endogenous AGEs produced by humans generate oxidative stress and activation of inflammatory signaling pathways via AGE-specific receptors. The present review summarizes current knowledge on the pathogenic role of AGEs in chronic noncommunicable diseases. Although correlations exist between glycation and the pathogenesis of these diseases, uncertainties remain in light of recurrent intervention failures of apparently promising animal models to be translated into clinically useful anti-AGE strategies. Future intervention of AGEs or their receptors should embrace more carefully executed clinical trials. Nevertheless, suppressing symptoms via lifetime drug application is unlikely to eliminate the burden of chronic diseases unless deep-rooted lifestyle issues that cause these diseases are simultaneously addressed.

中文翻译：

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高级糖化终产物的临床/转化方面

晚期糖基化终产物 (AGEs) 与慢性高血糖症和年龄相关疾病有关。人类产生的内源性AGEs通过AGE特异性受体产生氧化应激和炎症信号通路的激活。本综述总结了当前关于 AGEs 在慢性非传染性疾病中的致病作用的知识。尽管糖基化与这些疾病的发病机制之间存在相关性，但鉴于明显有希望转化为临床上有用的抗 AGE 策略的动物模型的反复干预失败，不确定性仍然存在。未来对 AGE 或其受体的干预应该包括更仔细地执行的临床试验。尽管如此，