Hepcidin and the iron enigma in HCV infection
Autor: | Eirini Karamichali, Alexios Dimitriadis, Pelagia Foka, Avgi Mamalaki, Urania Georgopoulou |
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Rok vydání: | 2014 |
Předmět: |
hepatitis C virus
Microbiology (medical) Hepatitis C virus Immunology cell signaling pathways Hepacivirus Review medicine.disease_cause Microbiology Pathogenesis Liver disease iron Immune system Hepcidins Hepcidin lipid metabolism medicine Animals Humans biology Transferrin saturation Hepatitis C Chronic medicine.disease Crosstalk (biology) Infectious Diseases Liver Infectious disease (medical specialty) biology.protein Parasitology hepcidin |
Zdroj: | Virulence |
ISSN: | 2150-5608 2150-5594 |
Popis: | An estimated 30–40% of patients with chronic hepatitis C have elevated serum iron, transferrin saturation, and ferritin levels. Clinical data suggest that iron is a co-morbidity factor for disease progression following HCV infection. Iron is essential for a number of fundamental metabolic processes in cells and organisms. Mammalian iron homeostasis is tightly regulated and this is maintained through the coordinated action of sensory and regulatory networks that modulate the expression of iron-related proteins at the transcriptional and/or posttranscriptional levels. Disturbances of iron homeostasis have been implicated in infectious disease pathogenesis. Viruses, similarly to other pathogens, can escape recognition by the immune system, but they need iron from their host to grow and spread. Hepcidin is a 25-aa peptide, present in human serum and urine and represents the key peptide hormone, which modulates iron homeostasis in the body. It is synthesized predominantly by hepatocytes and its mature form is released in circulation. In this review, we discuss recent advances in the exciting crosstalk of molecular mechanisms and cell signaling pathways by which iron and hepcidin production influences HCV-induced liver disease. |
Databáze: | OpenAIRE |
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