| Project/Area Number |
25860605
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Cardiovascular medicine
|
|---|
| Research Institution | The University of Tokushima |
|---|
Principal Investigator |
ISE Takayuki 徳島大学, 大学病院, 助教 (90621649)
|
|---|
| Project Period (FY) |
2013-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
|---|
| Keywords | 大動脈瘤 / Acute Aortic Syndrome / Acute Aortic Symdrome |
|---|
| Outline of Final Research Achievements |
Progression of aortic aneurysms often cause fatal events such as rupture and dissection.Thrombin has a crucial role in vascular remodelig through protease-activated receptor-1 activation in cardiac fibroblasts and cardiomyocytes. As heparin cofactor II (HCII) inhibits the action of tissue thrombin in the cardiovascular system, it is possible that HCII counteracts the development of vascular remodeling.We investigated the relationships between plasma HCII activity and presence of vascular disease, including aortic aneurusm, peripheral artery disease, coronary artery disease and cerebral artery disease.Plasma HCII activity was inversely associated with morbidity of vascular disease, including aortic aneurysm, peripheral artery disease, coronary artery disease and cerebral artery disease. This finding suggests that tissue thrombin inactivation by HCII is a novel therapeutic target for vascular remodeling and atherosclerosis.
|
