Patel Sanjeevkumar R, Dressler Gregory R
Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Trends Mol Med. 2005 Nov;11(11):512-8. doi: 10.1016/j.molmed.2005.09.007. Epub 2005 Oct 10.
Fibrosis, and in particular tubulointerstitial fibrosis, is a common feature of almost all chronic renal diseases. Over the past several years, significant progress has been made in defining the underlying mechanisms of tubulointerstitial fibrosis. In a variety of mouse models, expression of transforming growth factor-beta is a primary causative factor which leads to increased numbers of myofibroblasts, collagen deposition and loss of tubular epithelia. More recently, another member of the transforming growth factor-beta superfamily, BMP7, was shown to counteract transforming growth factor-beta-mediated fibrosis. The activities of these secreted factors are regulated, in part, by extracellular ligand binding proteins which can enhance or suppress receptor ligand interactions.
纤维化，尤其是肾小管间质纤维化，是几乎所有慢性肾脏疾病的共同特征。在过去几年中，在确定肾小管间质纤维化的潜在机制方面取得了重大进展。在多种小鼠模型中，转化生长因子-β的表达是导致肌成纤维细胞数量增加、胶原蛋白沉积和肾小管上皮细胞丢失的主要致病因素。最近，转化生长因子-β超家族的另一个成员BMP7被证明可对抗转化生长因子-β介导的纤维化。这些分泌因子的活性部分受细胞外配体结合蛋白的调节，这些蛋白可增强或抑制受体配体相互作用。
