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The Wnt/frizzled/GSK-3 beta pathway: a novel therapeutic target for cardiac hypertrophy

W Matthijs Blankesteijn1, Veerle A M van de Schans, Paul ter Horst

  • 1Department of Pharmacology and Toxicology, Cardiovascular Research Institute Maastricht, Maastricht University, P.O. Box 616, 6200MD Maastricht, The Netherlands. wm.blankesteijn@farmaco.unimaas.nl <wm.blankesteijn@farmaco.unimaas.nl>

Trends in Pharmacological Sciences
|March 18, 2008
PubMed

Insights

New research explores the Wnt/frizzled pathway

Area of Science:

  • Cardiovascular Biology
  • Molecular Signaling
  • Pharmacology

Background:

  • Cardiac hypertrophy, an excessive heart response to workload, is a major cause of heart failure.
  • Current treatments like renin-angiotensin system inhibitors and beta-blockers are insufficient for many patients.
  • Cardiac hypertrophy results from a balance between prohypertrophic and antihypertrophic pathways.

Purpose of the Study:

  • To review evidence on Wnt/frizzled signaling and glycogen synthase kinase-3 beta (GSK-3 beta) in cardiac hypertrophy.
  • To discuss the therapeutic potential of targeting the Wnt/frizzled/GSK-3 beta pathway for heart failure.

Main Methods:

  • Literature review of current research on Wnt/frizzled signaling.
  • Analysis of GSK-3 beta's role as an antihypertrophic factor.
  • Discussion of molecular mechanisms involving GSK-3 beta phosphorylation and sequestration.

Main Results:

  • GSK-3 beta possesses a significant antihypertrophic effect.
  • Growth factors and hypertrophic stimuli inhibit GSK-3 beta via phosphorylation at Ser9.
  • Wnt/frizzled pathway activation inactivates GSK-3 beta through sequestration.

Conclusions:

  • The Wnt/frizzled pathway and GSK-3 beta are key regulators of cardiac hypertrophy.
  • Targeting this pathway offers a promising novel therapeutic strategy for cardiac hypertrophy and heart failure.

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