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‘WNT-er is coming’: WNT signalling in chronic lung diseases
  1. H A Baarsma1,
  2. M Königshoff1,2
  1. 1 Comprehensive Pneumology Center, Helmholtz Center Munich, Ludwig Maximilians University Munich, University Hospital Grosshadern, Member of the German Center for Lung Research (DZL), Munich, Germany
  2. 2 Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado, USA
  1. Correspondence to Professor M Königshoff, Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, University of Colorado School of Medicine, Anschutz Medical Campus M/S C 272, 12700 E 19th Avenue, RC2, 9th Floor, Aurora, CO 80045-2581, USA; Melanie.Koenigshoff{at}


Chronic lung diseases represent a major public health problem with only limited therapeutic options. An important unmet need is to identify compounds and drugs that target key molecular pathways involved in the pathogenesis of chronic lung diseases. Over the last decade, there has been extensive interest in investigating Wingless/integrase-1 (WNT) signalling pathways; and WNT signal alterations have been linked to pulmonary disease pathogenesis and progression. Here, we comprehensively review the cumulative evidence for WNT pathway alterations in chronic lung pathologies, including idiopathic pulmonary fibrosis, pulmonary arterial hypertension, asthma and COPD. While many studies have focused on the canonical WNT/β-catenin signalling pathway, recent reports highlight that non-canonical WNT signalling may also significantly contribute to chronic lung pathologies; these studies will be particularly featured in this review. We further discuss recent advances uncovering the role of WNT signalling early in life, the potential of pharmaceutically modulating WNT signalling pathways and highlight (pre)clinical studies describing promising new therapies for chronic lung diseases.

  • Airway Epithelium
  • Asthma
  • COPD ÀÜ Mechanisms
  • Cytokine Biology
  • Idiopathic pulmonary fibrosis
  • COPD Pharmacology
  • Asthma Mechanisms

This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See:

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  • Twitter Follow Melanie Königshoff @m_konigshoff

  • Contributors HAB and MK conceptually designed and wrote the manuscript.

  • Funding HAB is supported by a postdoctoral fellowship from the European Respiratory Society (ERS Fellowship LTRF 79-2012) and a fellowship from Helmholtz Zentrum Germany (PFP PF-135). MK is supported by a European Research Council Starting Grant (ERC-StG-LS7, Grant No. 261302) and a W2/3 Professorship Award by the Helmholtz Association.

  • Competing interests None declared.

  • Provenance and peer review Commissioned; externally peer reviewed.

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