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WNT/β-catenin signaling in polycystic kidney disease

Anne Wuebken1, Kai M Schmidt-Ott

  • 1Max Delbrück Center for Molecular Medicine, Berlin, Germany.

Kidney International
|July 2, 2011
PubMed

Insights

WNT/β-catenin signaling was thought to cause cystic kidney diseases. However, new genetic mouse models show this is not always true, challenging the established view of cyst formation.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Genetics

Background:

  • Cystic kidney diseases are often associated with WNT signal transduction defects.
  • Aberrant WNT/β-catenin/TCF/Lef1 signaling and renal cyst formation are observed in mouse models.
  • This led to the hypothesis that WNT/β-catenin activation is a common cause of cystogenesis.

Purpose of the Study:

  • To investigate the role of WNT/β-catenin signaling in the pathogenesis of cystic kidney diseases.
  • To challenge the prevailing hypothesis regarding the universal involvement of WNT/β-catenin activation in cyst formation.

Main Methods:

  • Analysis of key genetic mouse models of cystic kidney disease.
  • Assessment of WNT/β-catenin activity in cyst-lining epithelia.

Main Results:

  • In contrast to previous findings, specific genetic mouse models of cystic kidney disease did not exhibit WNT/β-catenin activity in cyst-lining epithelia.
  • This suggests that WNT/β-catenin signaling is not universally required for cyst formation in all forms of cystic kidney disease.

Conclusions:

  • The hypothesis that WNT/β-catenin signaling activation is a common causative event in cystic kidney disease is challenged by new evidence.
  • Alternative or parallel pathways may be involved in the development of renal cysts.
  • Further research is needed to elucidate the diverse mechanisms underlying cystic kidney diseases.

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