P53 in kidney injury and repair: Mechanism and therapeutic potentials

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Chengyuan Tang1, Zhengwei Ma2, Jiefu Zhu1

  • 1Department of Nephrology, Key Laboratory of Kidney Disease and Blood Purification in Hunan, The Second Xiangya Hospital at Central South University, Changsha, Hunan, China.

Pharmacology & Therapeutics
|October 23, 2018
PubMed

Insights

Acute kidney injury (AKI) can lead to chronic kidney disease (CKD) due to incomplete repair. The tumor suppressor p53 influences AKI and repair, offering potential therapeutic targets for preventing CKD progression.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Oncology

Background:

  • Acute kidney injury (AKI) is a significant clinical issue with high mortality and contributes to chronic kidney disease (CKD).
  • Incomplete kidney repair following AKI is a key factor in the development of renal fibrosis and progression to CKD.
  • The tumor suppressor p53 is implicated in AKI and kidney repair processes like apoptosis, cell cycle arrest, and autophagy.

Purpose of the Study:

  • To review recent advances in understanding p53's role in AKI and kidney repair.
  • To identify the therapeutic potential of p53 in preventing AKI and its progression to CKD.
  • To outline future research directions concerning p53 in kidney disease.

Main Methods:

  • Literature review of studies investigating p53 in kidney injury and repair.
  • Analysis of molecular mechanisms underlying p53's function in renal pathophysiology.
  • Synthesis of current knowledge on p53 as a therapeutic target.

Main Results:

  • p53 plays a critical role in regulating cellular processes crucial for kidney repair after injury.
  • Dysregulation of p53 contributes to maladaptive repair, leading to fibrosis and CKD.
  • Understanding p53 mechanisms is vital for developing targeted therapies.

Conclusions:

  • p53 is a key regulator in AKI and kidney repair, influencing the transition to CKD.
  • Targeting p53 presents a promising strategy for treating AKI and preventing CKD.
  • Further research is needed to fully elucidate p53's mechanisms and therapeutic applications in kidney disease.
Keywords:
Acute kidney injuryApoptosisAutophagyCell cycleKidney repairRenal fibrosisp53

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