线粒体功能障碍在急性肾损伤向慢性肾脏疾病转变中的作用

Role of mitochondrial dysfunction in the transition of acute renal injury to chronic kidney disease

急性肾损伤(AKI)是一种发病率较高的临床综合征,会使远期慢性肾脏病(CKD)的发病率明显上升,其机制目前尚不完全明确,可能包括细胞周期停滞、小管上皮周围毛细血管变少、炎性细胞浸润等。线粒体功能障碍在其中的作用主要包括导致了过度氧化应激、促进炎性反应的发生及进展、直接诱导肾小管细胞凋亡等。

Acute kidney injury(AKI)is a clinical syndrome with a high incidence,which will significantly increase the incidence of chronic kidney disease(CKD).The mechanism of AKI-CKD transition is not clear.It may include cell cycle arrest,fewer capillaries around the tubule epithelium,inflammatory cell infiltration and so on.Mitochondrial dysfunction consequently leads to oxidative stress,inflammation response and renal tubular cell apoptosis resulting in AKI-CKD transition conclusively.