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      TGF-β and fibrosis in different organs — molecular pathway imprints

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          Abstract

          The action of transforming-growth-factor (TGF)-beta following inflammatory responses is characterized by increased production of extracellular matrix (ECM) components, as well as mesenchymal cell proliferation, migration, and accumulation. Thus, TGF-beta is important for the induction of fibrosis often associated with chronic phases of inflammatory diseases. This common feature of TGF-related pathologies is observed in many different organs. Therefore, in addition to the description of the common TGF-beta-pathway, this review focuses on TGF-beta-related pathogenetic effects in different pathologies/organs, i. e., arthritis, diabetic nephropathy, colitis/Crohn's disease, radiation-induced fibrosis, and myocarditis (including their similarities and dissimilarities). However, TGF-beta exhibits both exacerbating and ameliorating features, depending on the phase of disease and the site of action. Due to its central role in severe fibrotic diseases, TGF-beta nevertheless remains an attractive therapeutic target, if targeted locally and during the fibrotic phase of disease.

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          Author and article information

          Journal
          Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
          Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
          Elsevier BV
          09254439
          August 2009
          August 2009
          : 1792
          : 8
          : 746-756
          Article
          10.1016/j.bbadis.2009.06.004
          19539753
          6b6733dc-028c-4af5-86a8-dd0adb4b45a5
          © 2009

          https://www.elsevier.com/tdm/userlicense/1.0/

          https://www.elsevier.com/open-access/userlicense/1.0/

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