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November 17, 2016Cardiovascular ResearchOpen Access

The editorial summarizes that Axin2 is required to limit WNT/β-catenin signaling after birth, and its loss leads to progressive myxomatous extracellular matrix remodeling typical of human myxomatous valve disease.

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Population

Murine models (Axin2-/- mice and Fibrillin1+/C1039G mice)

Design

Editorial

Authors

SCSunita ChopraNANadia Al-SammarraieYLYimu Lai

Discussion

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Overview

Axin2 loss impairs valve maturation in animals; hypothesis-generating for myxomatous valve disease mechanisms in humans.

Structured PICO

P
Population
Murine models (Axin2-/- mice and Fibrillin1+/C1039G mice)

The editorial highlights new preclinical evidence that loss of Axin2 and subsequent hyperactivation of WNT/β-catenin signaling drives the pathogenesis of myxomatous valve disease.

Cite This Study

Chopra et al. (2016) studied this question.

synapsesocial.com/papers/6a70f99ea528af2d65c3d75ahttps://doi.org/10.1093/cvr/cvw236
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Modulation of Transforming Growth Factor-β Signaling and Extracellular Matrix Production in Myxomatous Mitral Valves by Angiotensin II Receptor Blockers2012 · 107 citations
  2. 2Loss of Axin2 results in impaired heart valve maturation and subsequent myxomatous valve disease2016 · 63 citations
  3. 3Nonbiased Molecular Screening Identifies Novel Molecular Regulators of Fibrogenic and Proliferative Signaling in Myxomatous Mitral Valve Disease2015 · 63 citations
  4. 4Wnt/β-catenin signaling enables developmental transitions during valvulogenesis2016 · 54 citations
  5. 5Loss of β-Catenin Promotes Chondrogenic Differentiation of Aortic Valve Interstitial Cells2014 · 60 citations