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• W38332512 endingPage "288S" @default.
• W38332512 startingPage "284S" @default.
• W38332512 abstract "Endothelin-1 (ET-1) production is increased in hypertrophied hearts accompanied with fibrosis. ET-1 is a potent mitogen of fibroblasts and ET receptor antagonists are reported to inhibit the proliferation of fibroblasts and cardiac fibrosis. Peroxisome-proliferator-activated receptor alpha (PPAR alpha), one of the nuclear hormone receptors, suppresses activator protein-1 (AP-1), one of the nuclear transcription factors. Activation of PPAR alpha is reported to inhibit thrombin-induced ET-1 production by repressing the AP-1 signalling pathway in vascular endothelial cells. We investigated effects of the PPAR alpha activator fenofibrate (80 mg/kg per day, per os) on mRNA levels of ET-1, collagen type I and type III and histological features of myocardial fibrosis in hypertrophied rat hearts due to pressure-overload by abdominal aortic banding (AB). The treatment with fenofibrate or vehicle was started 7 days before the AB operation. Four days after the AB operation, fenofibrate treatment significantly reduced ET-1 mRNA expression compared with vehicle treatment in AB rat hearts. Collagen type I and type III mRNA expression, and interstitial and perivascular fibrosis were attenuated in the fenofibrate-treated AB rat group. Since the ET-1 gene has AP-1 response elements in the 5'-flanking region, it is suggested that myocardial fibrosis is effectively inhibited by fenofibrate through suppression of AP-1-mediated ET-1 gene augmentation in the pressure-overloaded heart caused by aortic banding in rats." @default.
• W38332512 created "2016-06-24" @default.
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• W38332512 date "2002-09-01" @default.
• W38332512 modified "2023-10-16" @default.
• W38332512 title "Stimulation of peroxisome-proliferator-activated receptor α (PPAR α) attenuates cardiac fibrosis and endothelin-1 production in pressure-overloaded rat hearts" @default.
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• W38332512 doi "https://doi.org/10.1042/cs103s284s" @default.
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