Duodenal ferroportin is up-regulated in patients with chronic hepatitis C.
Duodenal ferroportin is up-regulated in patients with chronic hepatitis C.
复制标题
慢性丙型肝炎患者十二指肠铁转运蛋白上调
DOI:
10.1371/journal.pone.0110658
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发表时间:
2014
期刊:
影响因子:
3.7
通讯作者:
Yang J
中科院分区:
文献类型:
--
作者:
Ma L;Zou T;Yuan Y;Lv J;Dong X;Yang G;Zhu Y;Luo J;Zhang Z;Yang J
Hepatitis C virus (HCV) infection is a leading cause of liver-related mortality. Chronic hepatitis C (CHC) is frequently associated with disturbances in iron homeostasis, with serum iron and hepatic iron stores being elevated. Accumulating evidence indicates that chronic HCV infection suppresses expression of hepatic hepcidin, a key mediator of iron homeostasis, leading to iron overload conditions. Since hepcidin mediates degradation of ferroportin, a basolateral transporter involved in the release of iron from cells, diminished hepcidin expression probably leads to up-regulation of ferroportin-1 (Fpn1) in patients with CHC. In this study, we determined the protein levels of duodenal Fpn1, and found that its expression was significantly up-regulated in patients with CHC. The expression of duodenal Fpn1 is negatively correlated with mRNA levels of hepcidin, and positively correlated with serum iron parameters. Although iron is a critical factor for growth of a variety of pathogenic bacteria, our results suggest that iron overload in blood does not increase the infection rate of bacteria in patients with CHC.
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