细胞周期停滞:AKI向CKD转变的关键点  

Cell cycle arrest:a key point of AKI-to-CKD transition

作　　者：李慧霞 车若琛 张爱华[1,2] Li Huixia;Che Ruochen;Zhang Aihua(Children’s Hospital of Nanjing Medical University,Nanjing 210008,Jiangsu,China;Key Laboratory of Nanjing Medical University,Nanjing 210008,Jiangsu,China)

机构地区：[1]南京医科大学附属儿童医院,江苏南京210008 [2]南京医科大学重点实验室,江苏南京210008

出　　处：《生物医学转化》2021年第1期55-63,共9页Biomedical transformation

基　　金：国家自然科学基金重点项目(81830020)。

摘　　要：急性肾损伤(Acute Kidney Injury,AKI)向慢性肾脏病(Chronic Kidney Disease,CKD)的进展过程严重影响肾脏预后及患者生存质量,是目前研究热点之一,其中细胞周期停滞是AKI向CKD进展中一个重要的致病机制。其可能通过持续增加细胞因子及炎症因子生成和释放、上皮间充质转分化、细胞器应激/串扰、衰老激活、管周微血管稀疏等一系列适应性不良修复过程,加速AKI向CKD转变。故调控细胞周期有望成为预防、减缓甚至阻断AKI-CKD进展的新的靶点机制。As the major threat of poor renal outcome and survival quality,the mechanism of acute kidney injury(AKI)progressing to chronic kidney disease(CKD)has aroused much attention.The cell cycle arrest,one of the major culprits,accelerates the AKI-to-CKD transition through maladaptive repair that involved overwhelming cytokines excretion and inflammation storm,epithelial-mesenchymal transition,organelles stress/crosstalk,aging activation as well as peritubular capillary rarefaction.Therefore,the cell cycle regulation can serve as a novel potential therapeutic target for the prevention,alleviation and even interruption of AKI-to-CKD transition.

关 键 词：细胞周期停滞 G2/M期 急性肾损伤 慢性肾脏病 适应性不良修复 

分 类 号：R692[医药卫生—泌尿科学] R363.21[医药卫生—外科学]