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Review
. 2016 Dec;3(1):34.
doi: 10.1186/s40348-016-0062-6. Epub 2016 Oct 7.

Linking bronchopulmonary dysplasia to adult chronic lung diseases: role of WNT signaling

Chiharu Ota  1 , Hoeke A Baarsma  2 , Darcy E Wagner  2 , Anne Hilgendorff  2   3 , Melanie Königshoff  2
Affiliations
Review

Linking bronchopulmonary dysplasia to adult chronic lung diseases: role of WNT signaling

Chiharu Ota et al. Mol Cell Pediatr. 2016 Dec.

Abstract

Bronchopulmonary dysplasia (BPD) is one of the most common chronic lung diseases in infants caused by pre- and/or postnatal lung injury. BPD is characterized by arrested alveolarization and vascularization due to extracellular matrix remodeling, inflammation, and impaired growth factor signaling. WNT signaling is a critical pathway for normal lung development, and its altered signaling has been shown to be involved in the onset and progression of incurable chronic lung diseases in adulthood, such as chronic obstructive pulmonary disease (COPD) or idiopathic pulmonary fibrosis (IPF). In this review, we summarize the impact of WNT signaling on different stages of lung development and its potential contribution to developmental lung diseases, especially BPD, and chronic lung diseases in adulthood.

Keywords: Adult chronic lung diseases; Bronchopulmonary dysplasia (BPD); Lung development; WNT signaling.

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Figures

Fig. 1
Fig. 1
Overview of WNT/β-catenin signaling. Without WNT signaling (“WNT OFF”), “destruction complex phosphorylates cytosolic β-catenin and phosphorylated β-catenin is recognized and degraded by the proteasomes. With WNT signaling (“WNT ON”), the function of “destruction complex” is inhibited to phosphorylate cytosolic β-catenin. Then unphosphorylated β-catenin accumulates in the cytosol, translocates into the nucleus, and activates the WNT target gene expression, such as the T-cell factor and lymphoid enhancer factor-1 (TCF/LEF1) family of transcription factors
Fig. 2
Fig. 2
Developmental stages and the WNT/β-catenin signaling. In the embryonic stage (
See this image and copyright information in PMC

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