Transforming growth factor-beta gene transfer to the lung induces myofibroblast presence and pulmonary fibrosis.

作者: J. Gauldie , P. J. Sime , Z. Xing , B. Marr , G. M. Tremblay

DOI: 10.1007/978-3-642-58456-5_5

关键词:

摘要: Many cytokines have been implicated in the initiation or propagation of fibrogenesis. In particular, early-phase inflammatory cytokines, interleukin (IL) and tumor necrosis factor (TNF), members chemokine families, including IL monocyte chemotactic peptide (MCP-1) are known to be present inflamed tissue, both at beginning advanced stages fibrosis. addition, growth differentiating factors, such as fibroblast factors (FGFs), transforming (TGFs) platelet-derived (PDGFs) all pathogenesis fibrosis through their putative mode action demonstrated presence fibrotic tissue. Most data implicating various arises from studies involving immunohistochemistry detection gene expression within tissue vitro experiments showing activity on matrix formation by structural cells (fibroblasts, smooth-muscle cells, etc.).

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