Project/Area Number |
17H04178
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Cardiovascular medicine
|
Research Institution | Yamaguchi University |
Principal Investigator |
YANO Masafumi 山口大学, 大学院医学系研究科, 教授 (90294628)
|
Co-Investigator(Kenkyū-buntansha) |
小田 哲郎 山口大学, 医学部附属病院, 助教 (40569290)
山本 健 山口大学, 大学院医学系研究科, 教授 (50363122)
小林 茂樹 山口大学, 大学院医学系研究科, 准教授 (90397993)
|
Project Period (FY) |
2017-04-01 – 2020-03-31
|
Project Status |
Completed (Fiscal Year 2019)
|
Budget Amount *help |
¥16,770,000 (Direct Cost: ¥12,900,000、Indirect Cost: ¥3,870,000)
Fiscal Year 2019: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2017: ¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
|
Keywords | リアノジン受容体 / カルモジュリン / 心肥大 / 心不全 / 不整脈 / EC coupling |
Outline of Final Research Achievements |
We have succeeded in creating mice genetically invcreasing the affinity of calmodulin to ryanodine receptor. This mouse was able to suppress arrhythmia completely by mating with CPVT type KI mouse. There was almost no death from heart failure after TAC surgery, and cardiac hypertrophy did not occur while maintaining cardiac function. In clinical studies, the multicenter, double-blind, randomized SHO-IN trial demonstrating the efficacy of dantrolene for heart failure and severe arrhythmias currently has more than 150 enrolled cases.
|
Academic Significance and Societal Importance of the Research Achievements |
重症心不全における致死的不整脈を抑制するこれまでとは全く異なる方法を解明した。心肥大について、その機序にリアノジン受容体結合カルモジュリンの核内移行があるという全く新しい肥大の機序を明らかにした。さらに心肥大はなくても心機能は保たれ、よい代償性肥大などというものはないことを示した。
|