AGEs交联蛋白裂解剂的研究进展

葡萄糖和其他还原糖与蛋白的非酶糖基化反应导致晚期糖基化终产物(advanced glycosylation end products，AGEs)以及由AGEs引发的蛋白交联物的形成，这是糖尿病和衰老过程中引起并发症的主要原因。动物模型和临床前实验表明AGEs抑制剂以及AGEs交联结构裂解剂，如ALT-711，可以从不同的阶段打断AGEs的形成，特别是AGEs裂解剂能够逆转或软化由AGEs造成的组织、器官以及血管的硬化，因而有希望成为一类新型治疗药物，用于治疗糖尿病和衰老过程中由于AGEs引发的各种并发症。

Research progress of AGEs crosslinked protein breaker

Glucose and other reducing sugars react non-enzymatically with proteins, leading to the formation of advanced glycosylation end products (AGEs) and AGE-derived protein cross-linking. The accumulations of AGEs contribute to the pathological events leading to diabetic and aging complications. Animal model studies and preliminary clinical trials have revealed that AGEs-inhibitors and the cross-links breakers, such as ALT-711, can reduce the severity of pathological changes of advanced glycosylation at several stages, especially the AGEs breaker can reverse stiffening of body tissues, organs and vessels, thus offering new therapeutic approaches for glucose-derived complications of diabetes and ageing.