,Elevated expression of hepcidin post-renal ischemia reperfusion injury

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Numerous studies have demonstrated that ischemia reperfusion (I/R) injury is the main cause of acute renal failure in both native kidneys and allografts,which had a profound influence on both early and late function of a transplanted kidney [1].I/R injury causes the generation of high levels of free radicals composed mainly of reactive oxygen intermediates,and a sufficient concentration of free radicals is critical for the associated tissue damage.The mislocalized iron has been indicated to play an important role in this process [2,3],because these ions can mutagenize many types of molecules,including lipids,nucleotides,and the DNA backbone.Catalytic iron in urine,blood,and peroxidized lipids has been documented in acute renal failure mediated by hemoglobin and myoglobin [4].Hepcidin is an iron regulatory hormone mainly produced by hepatocytes in response to inflammatory stimuli,iron overload and hypoxia,and plays a key role in maintaining iron homeostasis [5,6].
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