Analysis of mechanism of anemia and iron deficiency in heart failure via hepcidin

2015 Fiscal Year Final Research Report

• Project/Area Number: 25461047
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Cardiovascular medicine
• Research Institution: Niigata University
• Principal Investigator: Hanawa Haruo 新潟大学, 医歯学系, 准教授 (40282983)
• Co-Investigator(Kenkyū-buntansha): 柏村 健 新潟大学, 医歯学総合病院, 助教 (70419290) ; 小澤 拓也 新潟大学, 医歯学系, 助教 (70467075)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 心不全 / 貧血 / 鉄欠乏 / ヘプシジン / 肝うっ血

Outline of Final Research Achievements

Anemia and iron deficiency are prevalent in patients with heart failure. The etiology of anemia and iron deficiency in heart failure patients is unclear. Hepcidin is known to be a main regulator of iron metabolism. The most frequent histopathologic finding in the liver of heart failure patients is congestion. Therefore, we speculated that liver congestion may induce the expression of hepcidin and result in exacerbated anemia. We prepared animal models with liver congestion and analyze mechanism of anemia and iron deficiency in heart failure via hepcidin. Our data indicated that liver congestion contributes to relative iron deficiency and anemia, and it does so via inappropriate expression of hepcidin. Moreover, our data in some patients with heart failure showed that the mechanism appeared.

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