急性肾损伤(AKI)是临床常见的急危重症之一,部分AKI患者进展为慢性肾脏病(CKD)。AKI向CKD转化的具体机制尚不十分清楚,涉及多个方面,如肾小球代偿性增大后硬化、肾间质炎症及纤维化、内皮功能损伤、肾小管管周毛细血管减少、氧化应激以及肾小管上皮细胞异常修复等。近年来研究发现AKI后肾小管上皮细胞异常修复是导致CKD的中心环节,而肾小管上皮细胞周期阻滞是上皮细胞异常修复的重要机制之一。本文就细胞周期阻滞在AKI向CKD转变中的机制进行综述。
Acute renal injury( AKI) is one of the most common severe acute diseases. Some patients with AKI may be likely to develop chronic kidney disease( CKD). However,the specific mechanism of CKD after AKI is not clear,which is associated with many factors,such as glomerular sclerosis after compensatory hyperplasia, renal interstitial inflammation and fibrosis,endothelial dysfunction,peritubular capillary rarefaction,oxidative stress and tubular epithelial cell abnormal repair. In recent years,it has been found that tubular epithelial cells abnormal repair after AKI plays a crucial role in developing CKD,and cell cycle arrest of tubular epithelial cells is one of the important mechanisms of epithelial cell abnormal repair. In this review,we summarized the recent advances in how cell cycle arrest links AKI to CKD.