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Gelsolin in idiopathic pulmonary fibrosis: a new target supports a central role for epithelial injury in disease pathogenesis
Correspondence to:
Professor M Whyte, Academic Unit of Respiratory Medicine, Department of Infection and Immunity, Faculty of Medicine, Dentistry and Health, University of Sheffield, Beech Hill Road, Sheffield S10 2RX, UK; m.k.whyte@sheffield.ac.uk
| The first 150 words of the full text of this article appear below. |
Idiopathic pulmonary fibrosis (IPF) is a highly heterogeneous condition and is likely to be initiated by many different forms of lung injury. Injury to the alveolar epithelium followed by aberrant repair is, however, recognised to be a central pathogenic mechanism in IPF.1 Histologically, there is evidence of epithelial cell hyperplasia and proliferation, particularly adjacent to fibroblastic foci, but also areas of epithelial apoptosis and denudation.2 In murine models of pulmonary fibrosis, inhibition of components of apoptotic signalling pathways abrogates both alveolar epithelial cell death and fibrosis. This has been achieved by treatment with caspase inhibitors or with antibody blockade of the Fas death receptor, these results being confirmed in mice deficient in murine Fas (lpr) or its ligand, gld.3 4 The mechanisms of epithelial cell apoptosis in human IPF are not clearly defined, although there is evidence that the Fas pathway may be upregulated resulting in caspase-dependent apoptosis.5 A recent paper
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Thorax 2009 64: 467-475.[Abstract] [Full Text] [PDF]
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