作者: Michael Zeisberg , Frank Strutz , Gerhard A. Müller
DOI: 10.1097/00041552-200105000-00004
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摘要: Tubulointerstitial fibrosis invariably accompanies the course of chronic renal failure towards end-stage disease. Tubular epithelial cells, predominant cell type in tubulointerstitium, are increasingly being recognized for playing a dominant role as mediators fibrogenesis. cells become activated either by glomerular ultrafiltrate from their apical side or mononuclear basolateral side. They initiate scarring process secreting chemokines, which return attract well growth factors that stimulate interstitial fibroblasts. In later phases fibrogenesis, cellular changes tubular contribute to impairment function. Whereas react proliferation hypertrophy initial stimuli, they may undergo apoptosis transdifferentiate into fibroblasts, and thus atrophy stages progressive Resident fibroblasts also important recent research has demonstrated these much more heterogeneous than expected. Cytokines such fibroblast factor 2 have been shown be pro-fibrogenic, whereas hepatocyte bone morphogenic protein 7 inhibit Despite progress, further is mandatory better understanding development novel therapeutic approaches.