Distinct Roles of Wnt/ β -Catenin Signaling in the Pathogenesis of Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis

Juan Shi; Feng Li; Meihui Luo; Jun Wei; Xiaoming Liu

doi:10.1155/2017/3520581

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Distinct Roles of Wnt/ β -Catenin Signaling in the Pathogenesis of Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis

Journal article

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Peer reviewed

Distinct Roles of Wnt/ β -Catenin Signaling in the Pathogenesis of Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis

Juan Shi, Feng Li, Meihui Luo, Jun Wei and Xiaoming Liu

Mediators of inflammation, Vol.2017, pp.3520581-16

2017

DOI: 10.1155/2017/3520581

PMCID: PMC5447271

PMID: 28588349

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Abstract

Wnt signaling pathways are tightly controlled under a physiological condition, under which they play key roles in many biological functions, including cell fate specification and tissue regeneration. Increasing lines of evidence recently demonstrated that a dysregulated activation of Wnt signaling, particularly the Wnt/ -catenin signaling, was involved in the pathogenesis of chronic pulmonary diseases, such as chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF). In this respect, Wnt signaling interacts with other cellular signaling pathways to regulate the initiation and pathogenic procedures of airway inflammation and remodeling, pulmonary myofibroblast proliferation, epithelial-to-mesenchymal transition (EMT), and development of emphysema. Intriguingly, Wnt/ -catenin signaling is activated in IPF; an inhibition of this signaling leads to an alleviation of pulmonary inflammation and fibrosis in experimental models. Conversely, Wnt/ -catenin signaling is inactivated in COPD tissues, and its reactivation results in an amelioration of airspace enlargement with a restored alveolar epithelial structure and function in emphysema models. These studies thus imply distinct mechanisms of Wnt/ -catenin signaling in the pathogenesis of these two chronic pulmonary diseases, indicating potential targets for COPD and IPF treatments. This review article aims to summarize the involvement and pathogenic roles of Wnt signaling pathways in the COPD and IPF, with a focus on the implication of Wnt/ -catenin signaling as underlying mechanisms and therapeutic targets in these two incurable diseases.

Animals

Pulmonary Disease, Chronic Obstructive - metabolism

Wnt Proteins - metabolism

beta Catenin - metabolism

Humans

Idiopathic Pulmonary Fibrosis - metabolism

Details

Title: Subtitle: Distinct Roles of Wnt/ β -Catenin Signaling in the Pathogenesis of Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis
Creators: Juan Shi - Center of Laboratory Medicine, General Hospital of Ningxia Medical University, Yinchuan 750004, China
Feng Li - Institute of Human Stem Cell Research, General Hospital of Ningxia Medical University, Yinchuan, Ningxia 750004, China
Meihui Luo - Center of Laboratory Medicine, General Hospital of Ningxia Medical University, Yinchuan 750004, China
Jun Wei - Institute of Human Stem Cell Research, General Hospital of Ningxia Medical University, Yinchuan, Ningxia 750004, China
Xiaoming Liu - Institute of Human Stem Cell Research, General Hospital of Ningxia Medical University, Yinchuan, Ningxia 750004, China
Resource Type: Journal article
Publication Details: Mediators of inflammation, Vol.2017, pp.3520581-16
DOI: 10.1155/2017/3520581
PMID: 28588349
PMCID: PMC5447271
NLM abbreviation: Mediators Inflamm
ISSN: 0962-9351
eISSN: 1466-1861
Publisher: United States
Grant note: DOI: 10.13039/501100001809, name: National Natural Science Foundation of China, award: 81460247, 31472191
Language: English
Date published: 2017
Academic Unit: Anatomy and Cell Biology
Record Identifier: 9984025465302771

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