Document Detail


Signaling pathways in the epithelial origins of pulmonary fibrosis.
MedLine Citation:
PMID:  20676040     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Pulmonary fibrosis complicates a number of disease processes and leads to substantial morbidity and mortality. Idiopathic pulmonary fibrosis (IPF) is perhaps the most pernicious and enigmatic form of the greater problem of lung fibrogenesis with a median survival of three years from diagnosis in affected patients. In this review, we will focus on the pathology of IPF as a model of pulmonary fibrotic processes, review possible cellular mechanisms, review current treatment approaches and review two transgenic mouse models of lung fibrosis to provide insight into processes that cause lung fibrosis. We will also summarize the potential utility of signaling pathway inhibitors as a future treatment in pulmonary fibrosis. Finally, we will present data demonstrating a minimal contribution of epithelial-mesenchymal transition in the development of fibrotic lesions in the transforming growth factor-alpha transgenic model of lung fibrosis.
Authors:
William D Hardie; James S Hagood; Vrushank Dave; Anne-Karina T Perl; Jeffrey A Whitsett; Thomas R Korfhagen; Stephan Glasser
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2010-07-03
Journal Detail:
Title:  Cell cycle (Georgetown, Tex.)     Volume:  9     ISSN:  1551-4005     ISO Abbreviation:  Cell Cycle     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-08-16     Completed Date:  2011-02-03     Revised Date:  2013-05-29    
Medline Journal Info:
Nlm Unique ID:  101137841     Medline TA:  Cell Cycle     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2769-76     Citation Subset:  IM    
Affiliation:
Department of Pediatrics, Pulmonary Medicine, University of California, San Diego, CA, USA. william.hardie@cchmc.org
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Disease Models, Animal
Epithelial Cells / cytology,  metabolism*
Humans
Mesoderm / cytology,  metabolism
Mice
Pulmonary Fibrosis / etiology*,  metabolism,  therapy
Pulmonary Surfactant-Associated Protein C / genetics,  metabolism
Receptor, Epidermal Growth Factor / metabolism
Signal Transduction*
Transforming Growth Factor beta / genetics,  metabolism
Grant Support
ID/Acronym/Agency:
AI58795/AI/NIAID NIH HHS; HL 082818/HL/NHLBI NIH HHS; HL086598/HL/NHLBI NIH HHS; HL50046/HL/NHLBI NIH HHS; HL61646/HL/NHLBI NIH HHS; HL90156/HL/NHLBI NIH HHS; R01 HL082818-03/HL/NHLBI NIH HHS; R01 HL082818-05/HL/NHLBI NIH HHS; R01 HL104003/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Pulmonary Surfactant-Associated Protein C; 0/Transforming Growth Factor beta; EC 2.7.10.1/Receptor, Epidermal Growth Factor
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Dasatinib alters the metastatic phenotype of B16-OVA melanoma in vivo.
Next Document:  Characterization of a novel mutation in the cardiac ryanodine receptor that results in catecholamine...