P53 in kidney injury and repair: Mechanism and therapeutic potentials

Chengyuan Tang, Zhengwei Ma, Jiefu Zhu, Zhiwen Liu, Yuxue Liu, Yu Liu, Juan Cai, Zheng Dong

Research output: Contribution to journalReview article

14 Scopus citations

Abstract

Acute kidney injury (AKI) is a major kidney disease with poor clinical outcome. Besides its acute consequence of high mortality, AKI may also contribute significantly to the occurrence and progression of chronic kidney diseases (CKD). Accumulating evidence has demonstrated that maladaptive and incomplete kidney repair after AKI leads to the development of renal fibrosis and, ultimately, CKD. p53, a well-known tumor suppressor, plays a critical role in AKI and subsequent kidney repair through the regulation of various cell biologic processes, including apoptosis, cell cycle arrest, and autophagy. Despite the notable progress in deciphering the involvement of p53 in kidney injury and repair, the underlying mechanisms of p53 in these pathological processes remain largely unknown. Further investigation in this area is essential for the application of p53 as therapeutic target to prevent and treat AKI or impede its progression to CKD. In this review, we summarize the recent advances in understanding p53 regulation of AKI and kidney repair, pinpoint the potential of p53 as a therapeutic target, and present future research interests and directions.

Original languageEnglish (US)
Pages (from-to)5-12
Number of pages8
JournalPharmacology and Therapeutics
Volume195
DOIs
StatePublished - Mar 2019

Keywords

  • Acute kidney injury
  • Apoptosis
  • Autophagy
  • Cell cycle
  • Kidney repair
  • Renal fibrosis
  • p53

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)

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