Role of carbon monoxide and biliverdin in renal ischemia/reperfusion injury.
Heme oxygenase (HO) isoforms catalyze the conversion of heme to carbon monoxide (CO) and biliverdin/bilirubin with a concurrent release of iron. There is strong evidence that HO activity and products play a major role in renoprotection, however the exact molecular mechanisms underlying the beneficial effects exerted by this pathway are not fully understood. This review is aimed at illustrating the possible mechanism/s by which HO is renoprotective in the context of ischemia/reperfusion. We will first analyze the effects of exogenous administration of bilirubin/biliverdin and CO and then describe their biological activities once generated endogenously following stimulation of the HO pathway by either pharmacological means or gene targeting-mediated approaches.
Li Volti
G
G
Division of Human Anatomy, Department of Biomedical Sciences and Biotechnology, University of Brescia, Brescia, Italy. livolti@unict.it
Rodella
L F
LF
Di Giacomo
C
C
Rezzani
R
R
Bianchi
R
R
Borsani
E
E
Gazzolo
D
D
Motterlini
R
R
D000818:Animals; D001663:Bilirubin / Q000502:physiology; D001664:Biliverdine / Q000502:physiology*; D002248:Carbon Monoxide / Q000502:physiology*; D006419:Heme Oxygenase (Decyclizing) / Q000378:metabolism*; D006801:Humans; D007668:Kidney / Q000098:blood supply*; D015427:Reperfusion Injury / Q000503:physiopathology*
D002248:Carbon Monoxide; D006419:Heme Oxygenase (Decyclizing); D001664:Biliverdine; D001663:Bilirubin