期刊论文详细信息
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE 卷:1792
TGF-β and fibrosis in different organs - molecular pathway imprints
Review
Pohlers, Dirk1  Brenmoehl, Julia2  Loeffler, Ivonne3  Mueller, Cornelia K.4  Leipner, Carola5  Schultze-Mosgau, Stefan4  Stallmach, Andreas2  Kinne, Raimund W.1  Wolf, Gunter3 
[1] Univ Jena, Expt Rheumatol Unit, Univ Hosp Jena, Waldkrankenhaus Rudolf Elle Eisenberg,Dept Orthop, Jena, Germany
[2] Univ Jena, Dept Gastroenterol Hepatol & Infect Dis, Clin Internal Med 2, Univ Hosp Jena, Jena, Germany
[3] Univ Jena, Univ Hosp Jena, Clin Internal Med 3, Jena, Germany
[4] Univ Jena, Univ Hosp Jena, Clin Oromaxillofacial Surg Plast Surg, Jena, Germany
[5] Univ Jena, Univ Hosp Jena, Anim Res Inst, Jena, Germany
关键词: TGF-beta;    Fibrosis;    Arthritis;    Nephritis;    Inflammatory bowel disease;    Crohn's disease;    Wound-healing;    Myocarditis;   
DOI  :  10.1016/j.bbadis.2009.06.004
来源: Elsevier
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【 摘 要 】

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 myrocarditis (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. (C) 2009 Elsevier B.V. All rights reserved.

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