| Project/Area Number |
22790737
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Hyogo Medical University |
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Principal Investigator |
NAITO Yoshiro 兵庫医科大学, 医学部, 講師 (10446049)
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|---|
| Project Period (FY) |
2010 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
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| Keywords | 循環器・高血圧 / 内科 / 基礎 / 高血圧・循環器 |
|---|
| Research Abstract |
We revealed that angiotensin II type 1a receptor(AT1aR) and erythropoietin receptor(EpoR) signal pathways are involved in the mechanism of iron deficiency induced cardiac remodeling. Dietary iron-restricted EpoR rescued mice, which express EpoR only in the hematopoietic lineage, demonstrated anemia and systolic dysfunction, thereby inducing heart failure and decreasing a survival rate. On the other hand, AT1aR knock-out mice attenuated Epo secretion in response to iron deficiency. As a result, our data suggests that modulation of AT1aR and cardiac EpoR signaling may represent a therapeutic target for anemia-induced heart failure.
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