| Project/Area Number |
22590815
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Circulatory organs internal medicine
|
|---|
| Research Institution | Kinki University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
ONO Koh 京都大学, 医学研究科, 講師 (00359275)
KOSHIMIZU Taka-aki 自治医科大学, 医学部, 准教授 (20392491)
|
|---|
| Project Period (FY) |
2010 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2010: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
|---|
| Keywords | 分子心臓病態学 / 心肥大 / 線維化 / 心不全 |
|---|
| Research Abstract |
We elucidated two novel mechanism in cardiac fibrosis. First, we have shown that metastasis-associated protein, S100A4 mediates pathological cardiac fibrosis through the modulation of p53 in cardiac fibroblast. Second, we have shown that the activation of vasopressin type 1a receptor contributes to the profibrotic effect of angiotensin II in the heart as well as the fibrosis and onset of heart failure seen in pressure-overloaded LV for the first time. In the future, we will investigate whether the modulation of these two factors may offer therapeutic benefits in heart failure.
|
