| Project/Area Number |
25461115
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Cardiovascular medicine
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| Research Institution | Nara Medical University |
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Principal Investigator |
TAKEDA YUKIJI 奈良県立医科大学, 医学部, 研究員 (60398443)
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| Co-Investigator(Kenkyū-buntansha) |
SAITO Yoshihiko 奈良県立医科大学, 医学部第1内科, 教授 (30250260)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | 心腎連関 / 可溶性Flt-1 / PLGF / 心不全 / 肺水腫 / Flt-1 / 慢性腎臓病 / 心室リモデリング / sFlt-1 |
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| Outline of Final Research Achievements |
Cardiac hypertrophy and heart failure are highly associated with chronic kidney diseases (CKD), by which mechanism is not fully understood.
The present study showed that production of PLGF is up-regulated and and a soluble form of its receptor, fms-like tyrosine kinase, is down-regulated in CKD.
Given that sFlt-1 acts as an endogenous antagonist against PLGF, the present study also provides the evidence that the imbalance of PLGF and sFlt-1production enhances the biological signaling pathway via Flt-1, and is involved in the cardiac hypertrophy and heart failure associated with CKD, via relative activation of the PLGF/Flt-1 pathway, using mice specifically lacking sFlt-1 but not Flt-1. These findings raise the possibility that the treatment strategy, inhibiting PLGF action or enhancing sFLt-1 production, is useful for the treatment of hypertrophy and heart failure in CKD.
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