2016 Fiscal Year Final Research Report
Elucidation of the mechanism of arrhythmia basement formation by oxidative stress and electrical myocardial regeneration therapy by Sema3A
| Project/Area Number |
25860617
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Cardiovascular medicine
|
|---|
| Research Institution | Nihon University (2014-2016)
Kitasato University (2013) |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2013-04-01 – 2017-03-31
|
| Keywords | 電気的リモデリング / 酸化ストレス / セマフォリン3A / イソプロテレノール |
|---|
| Outline of Final Research Achievements |
This study aims to experimentally verify the fundamental therapy for arrhythmia induced by oxidative stress.
Experiments using heterozygous heart/muscle-specific manganese superoxide-deficient mice revealed that myocardial hyper-oxidative stress reduces the expression of potassium channel-related factors, including fetal protein, and causes electrical remodeling. The research results were reported as a paper presentation. In addition, we started a therapeutic intervention study with semaphorin 3A (Sema3A), a fetal protein regulator, using the isoproterenol (ISP)-loaded myocardial mouse model. We have confirmed myocardial remodeling due to ISP and we plan to verify the therapeutic effects of Sema3A.
|
| Free Research Field |
医歯薬学
|
