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Am. J. Respir. Cell Mol. Biol. 42, 21-31 (2010)
The WNT family of signaling proteins is essential to organ development in general and lung morphogenesis in particular. Originally identified as a developmentally active signaling pathway, the WNT pathway has recently been linked to the pathogenesis of important lung diseases, in particular lung cancer and pulmonary fibrosis. This review summarizes our current understanding about WNT signaling in lung development and disease, and is structured into three chapters. The first chapter presents an introduction to WNT signaling, outlining WNT proteins, their receptors and signaling intermediates, as well as the regulation of this complex pathway. The second chapter focuses on the role of WNT signaling in the normal embryonic and adult lung, and highlights recent findings of altered WNT signaling in lung diseases, such as lung cancer, pulmonary fibrosis, or pulmonary arterial hypertension. In the last chapter, we will discuss novel data and ideas about the biological effects of WNT signaling on the cellular level, highlighting pleiotropic effects induced by WNT ligands on distinct cell types, and how these cellular effects may be relevant to the pathogenesis of the aforementioned diseases.
Impact Factor
Scopus SNIP
Web of Science
Times Cited
Times Cited
Scopus
Cited By
Cited By
Altmetric
4.477
1.330
204
214
Anmerkungen
Besondere Publikation
Auf Hompepage verbergern
Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Review
Schlagwörter
b-catenin; epithelial cell; lung cancer; lung fibrosis; epithelial-to-mesenchymal transition
Sprache
englisch
Veröffentlichungsjahr
2010
Prepublished im Jahr
2009
HGF-Berichtsjahr
2010
ISSN (print) / ISBN
1044-1549
e-ISSN
1535-4989
Quellenangaben
Band: 42,
Heft: 1,
Seiten: 21-31
Verlag
American Thoracic Society
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Lung Health and Immunity (LHI)
POF Topic(s)
30202 - Environmental Health
Forschungsfeld(er)
Lung Research
PSP-Element(e)
G-505000-003
WOS ID
WOS:000273204500005
Erfassungsdatum
2009-12-31