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

• Published in: Biochimica et biophysica acta Vol. 1792; no. 8; pp. 746 - 756
• Main Authors: Pohlers, Dirk, Brenmoehl, Julia, Löffler, Ivonne, Müller, Cornelia K., Leipner, Carola, Schultze-Mosgau, Stefan, Stallmach, Andreas, Kinne, Raimund W., Wolf, Gunter
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01-08-2009; Elsevier
• Subjects: Animals; Arthritis; Arthritis, Rheumatoid - metabolism; Arthritis, Rheumatoid - pathology; Crohn's disease; Diabetic Nephropathies - metabolism; Diabetic Nephropathies - pathology; Fibrosis; Fibrosis - metabolism; Fibrosis - pathology; Humans; Inflammation - metabolism; Inflammation - pathology; Inflammatory bowel disease; Intestines - immunology; Intestines - pathology; Myocarditis; Myocarditis - metabolism; Myocarditis - pathology; Nephritis; Radiation, Ionizing; Signal Transduction - physiology; TGF-β; Transforming Growth Factor beta - metabolism; Wound-healing; Inflammatory bowel disease; Myocarditis; Nephritis; Fibrosis; TGF-β; Arthritis; Crohn's disease; Wound-healing; nephritis; arthritis; myocarditis; fibrosis; inflammatory bowel disease; wound-healing
• ISSN: 0925-4439; 0006-3002; 1879-260X
• DOI: 10.1016/j.bbadis.2009.06.004

The action of transforming-growth-factor (TGF)-β following inflammatory responses is characterized by increased production of extracellular matrix (ECM) components, as well as mesenchymal cell proliferation, migration, and accumulation. Thus, TGF-β 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-β-pathway, this review focuses on TGF-β-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-β 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-β nevertheless remains an attractive therapeutic target, if targeted locally and during the fibrotic phase of disease.