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醛固酮与纤溶酶原激活物抑制剂-1:对肾损伤的影响

Aldosterone and PAI-1: implications for renal injury.

作者信息

Brown Nancy J, Vaughan Douglas E, Fogo Agnes B

机构信息

Deaprtment of Medicine, Vanderbilt University, Nashville, TN, USA.

出版信息

J Nephrol. 2002 May-Jun;15(3):230-5.

Abstract

Aldosterone modulates cardiovascular and renal injury and fibrosis in animal models. This review explores the hypothesis that aldosterone causes injury and fibrosis, in part, through effects on plasminogen activator inhibitor-1, the major physiological inhibitor of plasminogen activators in vivo. Aldosterone interacts with angiotensin II to increase plasminogen activator inhibitor-1 expression in vitro and in vivo. Plasminogen activator inhibitor-1, by inhibiting the production of plasmin from plasminogen, tips the balance in favor of extracellular matrix accumulation and promotes fibrosis. Aldosterone receptor antagonism decreases both PAI-1 expression and fibrosis in animal models. These findings have implications for the clinical management of cardiovascular and renal disease.

摘要

醛固酮可调节动物模型中的心血管和肾脏损伤及纤维化。本综述探讨了这样一种假说,即醛固酮导致损伤和纤维化,部分原因是其对纤溶酶原激活物抑制剂-1(体内纤溶酶原激活物的主要生理抑制剂)产生影响。醛固酮在体外和体内均与血管紧张素II相互作用,以增加纤溶酶原激活物抑制剂-1的表达。纤溶酶原激活物抑制剂-1通过抑制纤溶酶原产生纤溶酶,使平衡倾向于细胞外基质积聚并促进纤维化。在动物模型中,醛固酮受体拮抗作用可降低PAI-1表达和纤维化程度。这些发现对心血管和肾脏疾病的临床管理具有重要意义。

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