晚期糖基化终末产物及其受体在原发性高血压中的作用机制

Pathophysiologic Mechanisms of Advanced Glycation End Products and Their Receptors in Primary Hypertension

近年来研究发现晚期糖基化终末产物（advanced glycation end products，AGEs）在原发性高血压的发生、发展过程中起着一定的病理作用，AGEs主要通过直接修饰蛋白、结合受体RAGE并激活信号转导通路两条作用途径来发挥效应。此外AGEs—RAGE还与肾素-血管紧张素系统、氧化应激三者构成正反馈环路，共同参与了原发性高血压的进程。相信随着对AGEs—RAGE作剧机制及药物干预的进一步研究，抗AGEs的治疗策略将有望成为防治高血压及其并发症的新方向。

Recent studies suggested that advanced glycation end products （AGEs） may play a pathological role in the development of primary hypertension. AGEs can cause the modification of proteins directly. And AGEs - RAGE binding leads to the activation of several signal pathways. AGEs - RAGE, renin - angiotensin system and oxidative stress constitute a positive feedback loop and participate in the pathogenesis of primary hypertension. Treatment strategies of anti - AGEs will provide the new guidelines for the further treatment of primary hypertension and its complications.