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多种慢性肾脏疾病的共同病理特征是肾小球及肾小管间质的纤维化 ,TGF β和ANGⅡ都是该过程中有重要意义的生物活性因子。近年发现 ,ANGⅡ和TGF β之间有紧密的相互作用。在体外 ,ANGⅡ可诱导肾近曲小管上皮细胞及系膜细胞TGF β的表达 ;对多种慢性肾病动物模型的研究又发现这种作用在体内同样存在。用ACEI或 /和AT1RA阻断ANGⅡ的作用可使肾内TGF β表达下降 ,但不是完全恢复正常 ,因而也只能延缓而不是阻止疾病的进展。而在传统治疗的基础上合用独立针对TGF β的阻断剂 ,可能会真正阻断肾病的进展。
The common pathological features of a variety of chronic kidney diseases are glomerular and tubular interstitial fibrosis, both of which are important bioactive factors in this process. In recent years, ANG Ⅱ and TGF β have found close interaction. In vitro, angiotensin Ⅱ induced the expression of TGFβ in renal proximal tubule epithelial cells and mesangial cells. The study of various animal models of chronic kidney disease also found that this effect exists in vivo. Inhibition of ANG II by ACEI or / and AT1RA reduces renal TGFβ expression but does not completely return to normal and therefore delays but not halts the progression of the disease. In the traditional treatment based on the combined use of independent TGF beta blockers, may really block the progress of kidney disease.