基础医学与临床 ›› 2021, Vol. 41 ›› Issue (4): 589-592.

• 短篇综述 • 上一篇    下一篇

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

张欣, 廖晓辉*   

  1. 重庆医科大学附属第二医院 肾内科, 重庆 400010
  • 收稿日期:2020-08-28 修回日期:2020-12-20 出版日期:2021-04-05 发布日期:2021-04-05
  • 通讯作者: *lxh@hospital.cqmu.edu.cn
  • 基金资助:
    国家自然科学基金(81873604)

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

ZHANG Xin, LIAO Xiao-hui*   

  1. Department of Nephrology, the Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China
  • Received:2020-08-28 Revised:2020-12-20 Online:2021-04-05 Published:2021-04-05
  • Contact: *lxh@hospital.cqmu.edu.cn

摘要: 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。

关键词: 急性肾损伤, 慢性肾脏病, 线粒体, 氧化应激反应

Abstract: 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.

Key words: acute kidney injury, chronic kidney disease, mitochondrion, oxidative stress

中图分类号: