AASLD Abstract (pp. 162A–266A)
Autor: | Margaret M. Walters, Linda M. Fletcher, T. L. Murphy, Kim R. Bridle, Darrell H. G. Crawford |
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Rok vydání: | 2004 |
Předmět: |
chemistry.chemical_classification
congenital hereditary and neonatal diseases and abnormalities Messenger RNA Reactive oxygen species Hepatology biology Chemistry nutritional and metabolic diseases medicine.disease_cause Cell biology Downregulation and upregulation Hepcidin hemic and lymphatic diseases Gene expression biology.protein medicine Ethanol metabolism Transcription factor Oxidative stress |
Zdroj: | Hepatology. 40:676A-735A |
ISSN: | 1527-3350 0270-9139 |
DOI: | 10.1002/hep.1840400508 |
Popis: | Introduction: Oxidative stress plays a pivotal role in the pathogenesis of alcoholic liver disease (ALD). Iron homeostasis has been reported to be altered in ALD and available free iron may catalyse reactions generating reactive oxygen species (ROS). Hepcidin, a liver-derived circulating peptide, is pivotal in regulating iron homeostasis. We have previously shown that hepcidin mRNA is significantly downregulated in an animal model of ALD. The gene expression of CCAAT/enhancer-binding protein alpha (C/EBPa), a transcription factor which has been show to be a key regulator of hepcidin gene transcription, has also been reported to be modulated by alcohol.Conclusion: Endogenously produced ROS may be important modulators of hepcidin and C/EBPa gene expression. Inhibiting the formation of ROS increases hepcidin and C/EBPa mRNA expression. ROS produced from alcohol metabolism may play an important role in the suppression of hepcidin gene expression and this is possibly mediated in part via the transcription factor C/EBPa. |
Databáze: | OpenAIRE |
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