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• W2123093884 abstract "Objectives— Reduced fibrinolytic activity is associated with adverse cardiovascular events. Although insulin-regulated aminopeptidase (IRAP) was recently identified as the angiotensin (Ang) IV receptor (AT4R), the impact of AngIV-AT4R signaling distal to AngII on the activation of type-1 plasminogen activator inhibitor (PAI-1) in the fibrinolytic process and subsequent formation of thrombosis remains unclarified. Methods and Results— To determine whether AngIV would inhibit fibrinolysis via PAI-1 activation and promote thrombosis, we evaluated the degree of fibrinolysis in thrombosis models and investigated the roles of AT4R after vascular injury using IRAP knockout mice ( IRAP −/− ). In endothelial cells from control mice (WT; C57Bl6/J), both AngII and AngIV treatments increased PAI-1 mRNA expression in a dose-dependent manner, whereas the response was blunted in endothelial cells from IRAP −/− mice. FeCl 3 -induced thrombosis was suppressed in the carotid arteries of IRAP −/− mice when compared with WT mice. Similarly, in a model of carotid artery ligation and cuff placement, IRAP −/− mice demonstrated accelerated fibrinolysis 7 days after surgery and reduced occlusive thrombosis with negative remodeling at 28 days. Conclusions— AngIV-AT4R signaling has a key role in fibrinolysis and the subsequent formation of arterial thrombosis after vascular injury. AT4R may be a novel therapeutic target against cardiovascular disease." @default.
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• W2123093884 date "2009-12-01" @default.
• W2123093884 modified "2023-09-23" @default.
• W2123093884 title "Ablation of Angiotensin IV Receptor Attenuates Hypofibrinolysis via PAI-1 Downregulation and Reduces Occlusive Arterial Thrombosis" @default.
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• W2123093884 doi "https://doi.org/10.1161/atvbaha.109.195057" @default.
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