Đang chuẩn bị nút TẢI XUỐNG, xin hãy chờ
Tải xuống
Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: Evolving concepts of liver fibrogenesis provide new diagnostic and therapeutic options. | Comparative Hepatology BioMed Central Open Access Review Evolving concepts of liver fibrogenesis provide new diagnostic and therapeutic options Olav A Gressner Ralf Weiskirchen and Axel M Gressner Address Institute of Clinical Chemistry and Pathobiochemistry RWTH-University Hospital Aachen Germany Email Olav A Gressner - ogressner@ukaachen.de Ralf Weiskirchen - rweiskirchen@ukaachen.de Axel M Gressner - gressner@rwth-aachen.de Corresponding author Published 30 July 2007 Received 30 May 2007 Comparative Hepatology 2007 6 7 doi 10.1186 1476-5926-6-7 Accepted 30 July 2007 This article is available from http www.comparative-hepatology.cOm content 6 1 7 2007 Gressner et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http creativecommons.org licenses by 2.0 which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Despite intensive studies the clinical opportunities for patients with fibrosing liver diseases have not improved. This will be changed by increasing knowledge of new pathogenetic mechanisms which complement the canonical principle of fibrogenesis. The latter is based on the activation of hepatic stellate cells and their transdifferentiation to myofibroblasts induced by hepatocellular injury and consecutive inflammatory mediators such as TGF-p. Stellate cells express a broad spectrum of matrix components. New mechanisms indicate that the heterogeneous pool of myofibroblasts can be supplemented by epithelial-mesenchymal transition EMT from cholangiocytes and potentially also from hepatocytes to fibroblasts by influx of bone marrow-derived fibrocytes in the damaged liver tissue and by differentiation of a subgroup of monocytes to fibroblasts after homing in the damaged tissue. These processes are regulated by the cytokines TGF-P and BMP-7 chemokines colony-stimulating factors metalloproteinases and .
