Inhaltsangabe
The essential co-factor of endothelial nitric oxide synthase (eNOS) tetrahydrobiopterin (BH4) has been repeatedly shown to protect transplanted organs from ischemia reperfusion injury (IRI). So far, the underlying mechanism has not been described. One hypothesis is that BH4 treatment prevents disruption of the functional nitric oxide producing form of eNOS, the so-called "uncoupling" and related superoxide production, by sustaining the dimeric status of the enzyme. Herein we tested this hypothesis in a murine transplantation model.
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Über die Autorin bzw. den Autor
born 20.06.1985 in Leer (Ostfriesland), A Level at Ubbo-Emmius Gymnasium in Leer in June 2005, Studies of human medicine at Medical University of Innsbruck from 2006 to 2013, voluntary work at Daniel Swarovski Research Laboratory from 2010 to 2013, since Oktober 2013 internship in Anesthesiology at Schön Klinik München Harlaching
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Tetrahydrobiopterin in ischemia and reperfusion injury
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