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

被引:527
作者
Pohlers, Dirk [1 ]
Brenmoehl, Julia [2 ]
Loeffler, Ivonne [3 ]
Mueller, Cornelia K. [4 ]
Leipner, Carola [5 ]
Schultze-Mosgau, Stefan [4 ]
Stallmach, Andreas [2 ]
Kinne, Raimund W. [1 ]
Wolf, Gunter [3 ]
机构
[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
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2009年 / 1792卷 / 08期
关键词
TGF-beta; Fibrosis; Arthritis; Nephritis; Inflammatory bowel disease; Crohn's disease; Wound-healing; Myocarditis; GROWTH-FACTOR-BETA; INFLAMMATORY-BOWEL-DISEASE; EPITHELIAL-MESENCHYMAL TRANSITION; B3-INDUCED CHRONIC MYOCARDITIS; SMOOTH MUSCLE ACTIN; COLLAGEN-INDUCED ARTHRITIS; MATRIX GENE-EXPRESSION; PROXIMAL TUBULAR CELLS; FOCAL ADHESION KINASE; TUMOR-NECROSIS-FACTOR;
D O I
10.1016/j.bbadis.2009.06.004
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
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.
引用
收藏
页码:746 / 756
页数:11
相关论文
共 185 条
[1]   Transforming growth factor-β1 is up-regulated by podocytes in response to excess intraglomerular passage of proteins -: A central pathway in progressive glomerulosclerosis [J].
Abbate, M ;
Zoja, C ;
Morigi, M ;
Rottoli, D ;
Angioletti, S ;
Tomasoni, S ;
Zanchi, C ;
Longaretti, L ;
Donadelli, R ;
Remuzzi, G .
AMERICAN JOURNAL OF PATHOLOGY, 2002, 161 (06) :2179-2193
[2]   RAPID ONSET SYNOVIAL INFLAMMATION AND HYPERPLASIA INDUCED BY TRANSFORMING GROWTH FACTOR-BETA [J].
ALLEN, JB ;
MANTHEY, CL ;
HAND, AR ;
OHURA, K ;
ELLINGSWORTH, L ;
WAHL, SM .
JOURNAL OF EXPERIMENTAL MEDICINE, 1990, 171 (01) :231-247
[3]   Making sense of latent TGFβ activation [J].
Annes, JP ;
Munger, JS ;
Rifkin, DB .
JOURNAL OF CELL SCIENCE, 2003, 116 (02) :217-224
[4]  
[Anonymous], 1998, CURR PR MED
[5]   Imatinib as a novel antifibrotic agent in bleomycin-induced pulmonary fibrosis in mice [J].
Aono, Y ;
Nishioka, Y ;
Inayama, M ;
Ugai, M ;
Kishi, J ;
Uehara, H ;
Izumi, K ;
Sone, S .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2005, 171 (11) :1279-1285
[6]   Epithelial mesenchymal interactions in cancer and development [J].
Arias, AM .
CELL, 2001, 105 (04) :425-431
[7]   The compliance of collagen gels regulates transforming growth factor-β induction of α-smooth muscle actin in fibroblasts [J].
Arora, PD ;
Narani, N ;
McCulloch, CAG .
AMERICAN JOURNAL OF PATHOLOGY, 1999, 154 (03) :871-882
[8]   Expression of transforming growth factors alpha and beta in colonic mucosa in inflammatory bowel disease [J].
Babyatsky, MW ;
Rossiter, G ;
Podolsky, DK .
GASTROENTEROLOGY, 1996, 110 (04) :975-984
[9]   Growth factors in inflammatory bowel disease [J].
Beck, PL ;
Podolsky, DK .
INFLAMMATORY BOWEL DISEASES, 1999, 5 (01) :44-60
[10]   Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells [J].
Bettelli, E ;
Carrier, YJ ;
Gao, WD ;
Korn, T ;
Strom, TB ;
Oukka, M ;
Weiner, HL ;
Kuchroo, VK .
NATURE, 2006, 441 (7090) :235-238