Klahr S, Morrissey J J
Department of Internal Medicine, Washington University School of Medicine, Saint Louis, MO, USA.
Semin Nephrol. 1998 Nov;18(6):622-32.
Renal interstitial inflammation and fibrosis occurs after ureteral obstruction. Fibrosis most likely develops as a consequence of an imbalance between extracellular matrix synthesis and deposition and the degradation and removal of matrix. Angiotensin II is rapidly stimulated after the onset of ureteral obstruction. Angiotensin II in turn upregulates other factors (transforming growth factor beta, tumor necrosis factor-alpha, nuclear factor-kappaB, and several adhesion molecules and chemoattractants). Blockade of angiotensin II synthesis or inability of this peptide to bind to its receptor lessened the increased levels of mRNA for TGF-beta and collagen IV. Increased levels of angiotensin II have a major role in the development of tubulointerstitial fibrosis after ureteral obstruction.
输尿管梗阻后会发生肾间质炎症和纤维化。纤维化很可能是细胞外基质合成与沉积以及基质降解与清除之间失衡的结果。输尿管梗阻发作后，血管紧张素II会迅速受到刺激。血管紧张素II进而上调其他因子（转化生长因子β、肿瘤坏死因子-α、核因子-κB以及多种黏附分子和趋化因子）。血管紧张素II合成的阻断或该肽无法与其受体结合，会降低转化生长因子β和IV型胶原的mRNA水平升高。血管紧张素II水平升高在输尿管梗阻后肾小管间质纤维化的发展中起主要作用。
