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Increased expression of p21WAF1/CIP1 in kidney proximal tubules mediates fibrosis

Judit Megyesi1, Adel Tarcsafalvi2, Shenyang Li3

  • 1Division of Nephrology, University of Arkansas for Medical Sciences, Little Rock, Arkansas; Department of Physiology and Biophysics, University of Arkansas for Medical Sciences, Little Rock, Arkansas; and Central Arkansas Veterans Healthcare System, Little Rock, Arkansas.

American Journal of Physiology. Renal Physiology
|November 28, 2014
PubMed

Insights

Fibrosis, a cause of organ damage, depends on p21 expression after kidney injury. Blocking p21 induction may offer a new therapeutic strategy for fibrotic diseases.

Area of Science:

  • Nephrology
  • Cell Biology
  • Pathology

Background:

  • Tissue fibrosis is a significant cause of mortality, affecting organs like the kidney after injury.
  • Previous research indicated p21(WAF1/Cip1) is crucial for chronic kidney disease fibrosis.

Purpose of the Study:

  • To investigate the role of p21 in acute kidney injury-induced fibrosis.
  • To identify molecular mechanisms linking p21 to fibrosis.

Main Methods:

  • Utilized a renal ablation model for chronic kidney disease.
  • Induced acute kidney injury using two distinct methods.
  • Examined p21 expression in whole organs and specific kidney tubules.
  • Investigated transforming growth factor-β (TGF-β) induction in response to p21.

Main Results:

  • Both acute and chronic kidney injuries leading to fibrosis were dependent on p21 expression.
  • Restricting p21 expression to proximal tubules induced whole-organ fibrosis.
  • Transforming growth factor-β induction was identified as a fibrogenic pathway regulated by p21.

Conclusions:

  • Kidney fibrosis development is dependent on p21.
  • p21 acts as a molecular switch in fibrogenesis.
  • Inhibiting p21 induction post-stress presents a potential therapeutic target for fibrotic diseases.
Keywords:
cyclin-dependent kinase inhibitor 1Afibrosisp21proximal tubuletransforming growth factor-β

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