2010
DOI: 10.1007/s11033-010-0594-0
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Abstract: In idiopathic pulmonary fibrosis (IPF) patients the presence of missense polymorphisms (SNP) in members of the epidermal growth factor receptor (EGFR) family or their genetic association could influence the binding affinity of natural ligands, modifying the expression and the behavior of the correlated genes. EGFR family members are particularly involved in the epithelial injury and fibrotic process in IPF. Genetic variations in HER family of receptors may alter the possible therapeutic efficacy of EGFR inhibi… Show more

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Cited by 20 publications
(14 citation statements)
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“…Notably, a recent study confirms that the superstructure of galectins at the cell surface can bind cell-surface receptors such as epidermal growth factor receptor, which is a potent mitogen for collagen-producing mesenchymal cells (Partridge et al, 2004;Martinelli et al, 2011;Fuchs et al, 2014). Besides, Gal-3 exhibits high-affinity binding for the advanced glycosylation end product-binding proteins in macrophages, astrocytes, and endothelial cells.…”
Section: Cell Receptors and Ligandsmentioning
confidence: 83%
“…Notably, a recent study confirms that the superstructure of galectins at the cell surface can bind cell-surface receptors such as epidermal growth factor receptor, which is a potent mitogen for collagen-producing mesenchymal cells (Partridge et al, 2004;Martinelli et al, 2011;Fuchs et al, 2014). Besides, Gal-3 exhibits high-affinity binding for the advanced glycosylation end product-binding proteins in macrophages, astrocytes, and endothelial cells.…”
Section: Cell Receptors and Ligandsmentioning
confidence: 83%
“…Expression of both EGF and EGFR markedly increases in asthmatic airways (13) and has been shown to provide protection against epithelial injury by stimulating mucin production and inflammatory cell recruitment to the site of injury to initiate repair (64). However, other studies suggest that amphiregulin-dependent activation of EGFR can mediate development of pulmonary fibrosis through activation of fibroblast proliferation (260,580,642), that overexpression TGF-␤ correlates with development of idiopathic or bleomycin-induced pulmonary fibrosis (271,325,326,336), and that EGFR inhibitors reduce pulmonary fibrosis (209,239,562). Local release of AREG by human mast cells plays an important role in lung fibrosis by promoting the proliferation of primary human lung fibroblasts.…”
Section: Role Of Egfr In the Lungsmentioning
confidence: 99%
“…For example, increased expression of EGFR and TGF-␣, an EGFR ligand, were found in idiopathic pulmonary fibrosis patients and in the lungs of bleomycin-treated rats, an animal model of pulmonary fibrosis (18,19). TGF-␣ knock-out mice are protected from bleomycin-induced fibrosis whereas TGF-␣ over-expression in the murine lungs spontaneously induces progressive pulmonary fibrosis (20,21).…”
mentioning
confidence: 99%