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Query: UMLS:C0034069 (pulmonary fibrosis)
 7,050 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Growth factors are known not only to cause a mitogenic response and alter differentiated characteristics of the target cells, but also to play important roles in intercellular signaling. Many growth factors are expressed in the embryonic and regulate embryogenesis. Pulmonary fibrosis is characterized by a complex process involving chronic inflammatory reaction, fibroblast proliferation, and abnormal deposition of interstitial collagen as a result of excess healing reaction. In the early phases, TNF-alpha, IL-beta and GM-CSF secreted by alveolar macrophages regulate and enhance pulmonary inflammation. On the contrary, TGF-alpha, KGF and HGF have been reported to enhance repair of alveolar epithelium and vascular endothelium in the injured lung. Furthermore, growth factors produced by alveolar macrophages and epithelium, such as PDGF, TGF-beta and activin A and belongs to the TGF-beta supergene family are known to play cardinal roles in fibroblast proliferation and pulmonary fibrosis. Further works concerning this complex growth factors (cytokines) network are required to provide a basis of the pathophysiology of pulmonary fibrosis.
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PMID:[Growth factors in the process of inflammation and fibrosis in the lung]. 974 56

The recovery of an intact epithelium following lung injury is critical for restoration of lung homeostasis. The initial processes following injury include an acute inflammatory response, recruitment of immune cells, and epithelial cell spreading and migration upon an autologously secreted provisional matrix. Injury causes the release of factors that contribute to repair mechanisms including members of the epidermal growth factor and fibroblast growth factor families (TGF-alpha, KGF, HGF), chemokines (MCP-1), interleukins (IL-1beta, IL-2, IL-4, IL-13), and prostaglandins (PGE(2)), for example. These factors coordinate processes involving integrins, matrix materials (fibronectin, collagen, laminin), matrix metalloproteinases (MMP-1, MMP-7, MMP-9), focal adhesions, and cytoskeletal structures to promote cell spreading and migration. Several key signaling pathways are important in regulating these processes, including sonic hedgehog, Rho GTPases, MAP kinase pathways, STAT3, and Wnt. Changes in mechanical forces may also affect these pathways. Both localized and distal progenitor stem cells are recruited into the injured area, and proliferation and phenotypic differentiation of these cells leads to recovery of epithelial function. Persistent injury may contribute to the pathology of diseases such as asthma, chronic obstructive pulmonary disease, and pulmonary fibrosis. For example, dysregulated repair processes involving TGF-beta and epithelial-mesenchymal transition may lead to fibrosis. This review focuses on the processes of epithelial restitution, the localization and role of epithelial progenitor stem cells, the initiating factors involved in repair, and the signaling pathways involved in these processes.
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PMID:Epithelial repair mechanisms in the lung. 2036 51

TGF beta is a multifunctional cytokine that is important in the pathogenesis of pulmonary fibrosis. The ability of TGF beta to stimulate smooth muscle actin and extracellular matrix gene expression in fibroblasts is well established. In this report, we evaluated the effect of TGF beta on the expression of HGF, FGF7 (KGF), and FGF10, important growth and survival factors for the alveolar epithelium. These growth factors are important for maintaining type II cells and for restoration of the epithelium after lung injury. Under conditions of normal serum supplementation or serum withdrawal TGF beta inhibited fibroblast expression of HGF, FGF7, and FGF10. We confirmed these observations with genome wide RNA sequencing of the response of control and IPF fibroblasts to TGF beta. In general, gene expression in IPF fibroblasts was similar to control fibroblasts. Reduced expression of HGF, FGF7, and FGF10 is another means whereby TGF beta impairs epithelial healing and promotes fibrosis after lung injury.
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PMID:TGF beta inhibits HGF, FGF7, and FGF10 expression in normal and IPF lung fibroblasts. 3015 85