作者: Olav A. Gressner , Axel M. Gressner
DOI: 10.1111/J.1478-3231.2008.01826.X
关键词:
摘要: Connective tissue growth factor (CTGF=CCN2), one of six members cysteine-rich, secreted, heparin-binding proteins with a modular structure, is recognized as an important player in fibrogenic pathways deduced from findings non-hepatic tissues and emerging results liver fibrosis. Collectively, the data show strongly increased expression fibrosing transforming (TGF-beta)-stimulated hepatocytes, biliary epithelial cells stellate cells. Functional activity mediator fibre-fibre, fibre-matrix matrix-matrix interactions, enhancer profibrogenic TGF-beta several secondary effects owing to enhancement, down-modulator bioactivity bone morphogenetic protein-7 has been proposed. By changing ratio its antagonist bone-morphogenetic protein-7, CTGF proposed master switch for epithelial-mesenchymal transition. Consequently, knockdown considerably attenuates experimental The spill-over into blood stream proposes this protein non-invasive reporter organ. Indeed, CTGF-levels sera correlate significantly activity. suggest multifaceted regulatory fibrosis, which offers translational aspects diagnosis follow-up hepatic fibrogenesis target therapeutic interventions. In addition, CTGF-promoter polymorphism might be importance prognostic genetic marker predict progression