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血管紧张素Ⅱ在肾间质纤维化中的作用机制 被引量:5

The mechanism of action for AngiotensinⅡ in renal interstitial fibrosis
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摘要 慢性肾脏病进展是多因素的,与肾小球损伤相比,以细胞外基质(ECM)积聚为特征的肾脏间质纤维化更能够反映肾脏疾病的进展。肾素-血管紧张素系统(RAS)的激活是肾间质纤维化的一个关键因素,其中,血管紧张素Ⅱ(AngⅡ)是其主要的促纤维化因子。AngⅡ介导肾间质纤维化依赖于多种机制。通过了解AngⅡ在肾间质纤维化中的作用机制,将为慢性肾脏病提供新的治疗策略。 The cause of progression for chronic kidney acterized by the accumulation of extraeellular matrix disease (CKD) is muhifactorial. Renal interstitial fibrosis char- (ECM), is a better reveal of progression for CKD, compared to glomeruli damage. The activation of the renin-angiotensin system (RAS) is a key factor for renal interstitial fibrosis. Angiotensin Ⅱ (AngⅡ), the main effector of RAS, is a critical promoter of fibrogenesis, the mechanisms underlying its profibrogenic effects are complex. A better understanding of the effects of Ang Ⅱ for renal interstitial fibrosis, will con- tribute to developing better strategies for the CKD.
出处 《中国医药导报》 CAS 2017年第2期29-32,共4页 China Medical Herald
基金 国家自然科学基金青年基金项目(81500516)
关键词 血管紧张素Ⅱ 肾间质纤维化 转化生长因子Β1 Angiotensin Ⅱ Renal interstitial fibrosis Transforming growth factor-[51
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