1. Alterations in the redox state and liver damage: Hints from the EASL Basic School of Hepatology
- Author
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Claudio Tiribelli, Gianluca Tell, Carlo Vascotto, Tell, Gianluca, Vascotto, Carlo, and Tiribelli, Claudio
- Subjects
medicine.medical_specialty ,Redox proteomics ,medicine.disease_cause ,Redox ,03 medical and health sciences ,Liver disease ,0302 clinical medicine ,Human disease ,Internal medicine ,medicine ,Animals ,Humans ,Liver damage ,030304 developmental biology ,Inflammation ,0303 health sciences ,Hepatology ,business.industry ,Liver Diseases ,medicine.disease ,Cell function ,3. Good health ,Disease Models, Animal ,Italy ,Liver ,Oxidative stress ,030220 oncology & carcinogenesis ,Hereditary hemochromatosis ,Immunology ,Liver disease, Oxidative stress, Redox proteomics, Inflammation ,business ,Reactive Oxygen Species ,Neuroscience ,Oxidation-Reduction - Abstract
Summary The importance of a correct balance between oxidative and reductive events has been shown to have a paramount effect on cell function for quite a long time. However, in spite of this body of rapidly growing evidence, the implication of the alteration of the redox state in human disease has been so far much less appreciated. Liver diseases make no exception. Although not fully comprehensive, this article reports what discussed during an EASL Basic School held in 2012 in Trieste, Italy, where the effect of the alteration of the redox state was addressed in different experimental and human models. This translational approach resulted in further stressing the concept that this topic should be expanded in the future not only to better understand how oxidative stress may be linked to a liver damage but also, perhaps more important, how this may be the target for better, more focused treatments. In parallel, understanding how alteration of the redox balance may be associated with liver damage may help define sensitive and ideally early biomarkers of the disorder. Abbreviations: ROS, reactive oxygen species, RNS, reactive nitrogen species, SOD, superoxide dismutase, ALI, acute liver injuries, CLD, chronic liver diseases, HCC, hepatocarcinoma, HBV, hepatitis B virus, HCV, hepatitis C virus, NAFLD, non-alcoholic fatty liver disease, MDA, malondialdehyde, 4-HNE, 4-hydroxynonenal, APE1/Ref-1, apurinic apyrimidinic endonuclease/redox effector factor 1, TNF, tumor necrosis factor, NOS2, nitric oxide synthase 2, ETC, electron transport chain, I/R, ischemia/reperfusion, FA, fatty acids, NASH, non-alcoholic steatohepatitis, ASH, alcoholic steatohepatitis, 8OHdG, 8-hydrossyguanosine, HIF-1 α, hypoxia-inducible factor 1α, PHD, prolyl-hydroxylases, NF-κB, nuclear factor-κB, GSH, reduced glutathione, GSSG, oxidized glutathione, CVD, cardiovascular disease, ER, endoplasmic reticulum, ERS, endoplasmic reticulum stress, HH, hereditary hemochromatosis, MPO, myeloperoxidase, HLPP, Human Liver Proteome Project, 2-DE, two-dimensional electrophoresis, MS, mass spectrometry, LC, liquid chromatography Keywords: Liver disease, Oxidative stress, Redox proteomics, Inflammation
- Published
- 2013