Journal of Capital Medical University ›› 2022, Vol. 43 ›› Issue (5): 720-727.doi: 10.3969/j.issn.1006-7795.2022.05.009

• Clinical and Basic Research in Nephrology • Previous Articles     Next Articles

Progress on the injury and repair mechanism of renal tubular epithelial cells in the transition of acute kidney injury to chronic kidney disease

Chen Xiaomei, Ma Yuanyuan, Nie Jing, Zhu Fengxin*   

  1. Department of Nephrology ,Nanfang Hospital, Southern Medical University, Guangzhou 510000, China
  • Received:2022-05-09 Online:2022-10-21 Published:2022-10-25
  • Contact: * E-mail:zhufengxin@126.com
  • Supported by:
    Major Project of National Natural Science Foundation of China(82090023),Key Project of National Natural Science Foundation of China(81730019), National Natural Science Foundation of China(82170700).

Abstract: Acute kidney injury (AKI) is a clinical syndrome caused by various factors and characterized by renal function declines sharply in a short period of time. AKI, an independent risk factor of chronic kidney disease (CKD) and end-stage renal disease, is associated with high levels of morbidity and mortality. Currently, the treatments for AKI and the prevention of the transition of AKI to CKD are very limited. Therefore, it is essential to explore the mechanism of AKI to CKD. Renal tubular epithelial cells (RTECs) are the major cells of the kidney and are vulnerable to various biological stresses, such as ischemia, hypoxia and toxins.RTECs are also key inflammatory and fibrogenic cells that drive the progression from acute to chronic kidney disease. In view of the central role of RTECs, this review will focus on the maladaptive repair mechanisms of RTECs in the transition of AKI to CKD, providing novel targets and new strategies for effective treatment.

Key words: renal tubular epithelial cells, injury and repair, acute kidney injury, chronic kidney disease

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