Abstract
Ischemia-reperfusion injury is a primarily nonallospecific event leading to the depletion of the essential nitric oxide synthase cofactor and potent antioxidant tetrahydrobiopterin. Suboptimal concentrations of tetrahydrobiopterin result in a reduced biosynthesis of nitric oxide leading to vascular endothelial dysfunction. Tetrahydrobiopterin supplementation has been shown to protect from this pathological state in a plethora of cardiovascular diseases including transplant-related ischemia-reperfusion injury. Even though still controversially discussed, there is increasing evidence emerging from both human as well as animal studies that tetrahydrobiopterin-mediated actions rely on its nitric oxide synthase cofactor activity rather than on its antioxidative properties. Herein, we review the current literature regarding the role of tetrahydrobiopterin in ischemia-reperfusion injury including our experience acquired in a murine pancreas transplantation model.
Original language | English (US) |
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Pages (from-to) | 13-19 |
Number of pages | 7 |
Journal | Pteridines |
Volume | 24 |
Issue number | 1 |
DOIs | |
State | Published - Jun 2013 |
Keywords
- Animal model
- Ischemia-reperfusion injury
- Nitric oxide
- Organ transplantation
- Tetrahydrobiopterin
ASJC Scopus subject areas
- Biochemistry
- Molecular Medicine
- Clinical Biochemistry