Studies on molecular pathological network of vascular and valvular calcification in CKD and survey for therapeutic target
Project/Area Number |
15K09271
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Kidney internal medicine
|
Research Institution | Keio University |
Principal Investigator |
|
Co-Investigator(Renkei-kenkyūsha) |
YOSHIDA Tadashi 慶應義塾大学, 医学部, 准教授 (00306713)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | 慢性腎臓病 / 血管石灰化 / NFkB / NFκB |
Outline of Final Research Achievements |
In the patients with chronic kidney diseases (CKD), it is well known that vascular calcification induces various complications. In this study, we developed a mouse model to reveal the mechanisms of vascular calcification.In this model mouse, vascular smooth muscle cells in the aorta were shown to lose its phenotype and gain the characteristics of osteogenic cells in molecular level. In addition, this phenomenon was ameliorated in the mouse which lost NFkB activity (important protein for various inflammatory diseases). From these findings, it is strongly suggested that inhibitor for NFkB will be a good candidate for the prevention of vascular calcification in CKD.
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Report
(4 results)
Research Products
(8 results)