CAJ | 학술논문

晚期糖基化终末产物(AGEs)在体内的增加、蓄积会引起各种细胞功能障碍,促进糖尿病微血管并发症特别是糖尿病肾病的发生和发展.AGEs可引起肾脏功能障碍和结构改变.针对AGEs的药物如抑制AGEs形成的药物、AGEs交联裂解剂、阻断AGEs及其受体相互作用的药物、抑制AGEs受体的表达及其下游路径的药物,分别作用于不同的信号通路环节,但都具有减少AGEs对靶器官损伤的作用,对糖尿病肾病具有一定的治疗作用.
만기당기화종말산물(AGEs)재체내적증가、축적회인기각충세포공능장애,촉진당뇨병미혈관병발증특별시당뇨병신병적발생화발전.AGEs가인기신장공능장애화결구개변.침대AGEs적약물여억제AGEs형성적약물、AGEs교련렬해제、조단AGEs급기수체상호작용적약물、억제AGEs수체적표체급기하유로경적약물,분별작용우불동적신호통로배절,단도구유감소AGEs대파기관손상적작용,대당뇨병신병구유일정적치료작용.
Advanced glycation end products (AGEs) increased or accumulated in the body may get rise to cell dysfunction and promote diabetic microvascular complications,especially the development of diabetic nephropathy (DN).AGEs can cause the functional and structural changes of the kidney.Though focusing on different points of signal pathway,a number of new agents,such as inhibitors and breakers of AGEs,receptor antagonists for AGEs and inhibitors to the signal transduction pathway after AGEs receptor,can decrease the negative effect of AGEs on target organs and play therapeutic roles in DN.