| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| 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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