TGF-beta and fibrosis in different organs - molecular pathway imprints.
Dirk Pohlers, Julia Brenmoehl, Ivonne Löffler, Cornelia K Müller, Carola Leipner, Stefan Schultze-Mosgau, Andreas Stallmach, Raimund W Kinne, Gunter Wolf
Experimental Rheumatology Unit, Department of Orthopedics, Waldkrankenhaus Rudolf Elle Eisenberg, University Hospital Jena, Friedrich Schiller University, Jena, Germany.
Biochimica et biophysica acta 2009 AugThe 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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Dirk Pohlers, Julia Brenmoehl, Ivonne Löffler, Cornelia K Müller, Carola Leipner, Stefan Schultze-Mosgau, Andreas Stallmach, Raimund W Kinne, Gunter Wolf. TGF-beta and fibrosis in different organs - molecular pathway imprints. Biochimica et biophysica acta. 2009 Aug;1792(8):746-56
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PMID: 19539753
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