• Kuldeep Kumawat, Tim Koopmans, and Reinoud Gosens.
• University of Groningen, Groningen Research Institute for Asthma and COPD, Department of Molecular Pharmacology , A. Deusinglaan 1, 9713 AV Groningen , The Netherlands +31 50 363 8177 ; +31 50 363 6908 ; r.gosens@rug.nl.
• Expert Opin. Ther. Targets. 2014 Sep 1;18(9):1023-34.

IntroductionPathological alteration in the airway structure, termed as airway remodeling, is a hallmark feature of individuals with asthma and has been described to negatively impact lung function in asthmatics. Recent studies have raised considerable interest in the regulatory role of β-catenin in remodeling asthmatic airways. The WNT/β-catenin signaling pathway is the key to normal lung development and tightly coordinates the maintenance of tissue homeostasis under steady-state conditions. Several studies indicate the crucial role of β-catenin signaling in airway remodeling in asthma and suggest that this pathway may be activated by both the growth factors and mechanical stimuli such as bronchoconstriction.Areas CoveredIn this review, we discuss recent literature regarding the mechanisms of β-catenin signaling activation and its mechanistic role in asthmatic airway remodeling. Further, we discuss the possibilities of therapeutic targeting of β-catenin.Expert OpinionThe aberrant activation of β-catenin signaling by both WNT-dependent and -independent mechanisms in asthmatic airways plays a key role in remodeling the airways, including cell proliferation, differentiation, tissue repair and extracellular matrix production. These findings are interesting from both a mechanistic and therapeutic perspective, as several drug classes have now been described that target β-catenin signaling directly.

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