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A new direction in the pathogenesis of idiopathic pulmonary fibrosis?
A recent review article suggested that idiopathic pulmonary fibrosis (IPF) is a disease that is associated more with abnormal wound healing than with inflammation. Data derived from transgenic and gene transfer rodent models suggest that lung inflammation may be a necessary but insufficient componen...
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2002
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC64807/ https://www.ncbi.nlm.nih.gov/pubmed/11806836 http://dx.doi.org/10.1186/rr158 |
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author | Gauldie, Jack Kolb, Martin Sime, Patricia J |
author_facet | Gauldie, Jack Kolb, Martin Sime, Patricia J |
author_sort | Gauldie, Jack |
collection | PubMed |
description | A recent review article suggested that idiopathic pulmonary fibrosis (IPF) is a disease that is associated more with abnormal wound healing than with inflammation. Data derived from transgenic and gene transfer rodent models suggest that lung inflammation may be a necessary but insufficient component of IPF, and that at some point in the natural history of the disease IPF becomes no longer dependent on the inflammatory response for propagation. Altered microenvironment and involvement of epithelial cell/mesenchymal cell interaction are the most likely contributors to the pathogenesis of this chronic progressive disorder. |
format | Text |
id | pubmed-64807 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2002 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-648072002-01-25 A new direction in the pathogenesis of idiopathic pulmonary fibrosis? Gauldie, Jack Kolb, Martin Sime, Patricia J Respir Res Commentary A recent review article suggested that idiopathic pulmonary fibrosis (IPF) is a disease that is associated more with abnormal wound healing than with inflammation. Data derived from transgenic and gene transfer rodent models suggest that lung inflammation may be a necessary but insufficient component of IPF, and that at some point in the natural history of the disease IPF becomes no longer dependent on the inflammatory response for propagation. Altered microenvironment and involvement of epithelial cell/mesenchymal cell interaction are the most likely contributors to the pathogenesis of this chronic progressive disorder. BioMed Central 2002 2001-09-26 /pmc/articles/PMC64807/ /pubmed/11806836 http://dx.doi.org/10.1186/rr158 Text en Copyright © 2001 BioMed Central Ltd |
spellingShingle | Commentary Gauldie, Jack Kolb, Martin Sime, Patricia J A new direction in the pathogenesis of idiopathic pulmonary fibrosis? |
title | A new direction in the pathogenesis of idiopathic pulmonary fibrosis? |
title_full | A new direction in the pathogenesis of idiopathic pulmonary fibrosis? |
title_fullStr | A new direction in the pathogenesis of idiopathic pulmonary fibrosis? |
title_full_unstemmed | A new direction in the pathogenesis of idiopathic pulmonary fibrosis? |
title_short | A new direction in the pathogenesis of idiopathic pulmonary fibrosis? |
title_sort | new direction in the pathogenesis of idiopathic pulmonary fibrosis? |
topic | Commentary |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC64807/ https://www.ncbi.nlm.nih.gov/pubmed/11806836 http://dx.doi.org/10.1186/rr158 |
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