Tetrahydrobiopterin attenuates ischemiareperfusion injury following organ transplantation by targeting the nitric oxide synthase: Investigations in an animal model

Benno Cardini, Rupert Oberhuber, Sven R. Hein, Katrin Watschinger, Martin Hermann, Peter Obrist, Gabriele Werner-Felmayer, Gerald Brandacher, Johann Pratschke, Ernst R. Werner, Manuel Maglione

Research output: Contribution to journalReview article

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 languageEnglish (US)
Pages (from-to)13-19
Number of pages7
JournalPteridines
Volume24
Issue number1
DOIs
StatePublished - Jun 1 2013

Keywords

  • Animal model
  • Ischemia-reperfusion injury
  • Nitric oxide
  • Organ transplantation
  • Tetrahydrobiopterin

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Medicine
  • Clinical Biochemistry

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