2022 Fiscal Year Final Research Report
Molecular Mechanisms of Atrial Fibrillation Suppression by Leak K+ Current
| Project/Area Number |
20K16116
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 48020:Physiology-related
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| Research Institution | Akita University |
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Principal Investigator |
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| Project Period (FY) |
2020-04-01 – 2023-03-31
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| Keywords | 心房性不整脈 / リークK電流 / ノックアウトマウス |
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| Outline of Final Research Achievements |
In a rat model of induced atrial arrhythmias, activation of leaky K currents suppresses arrhythmias. In conditioned knockout (CKO) mice of the leaky K channel, atrial arrhythmias were observed to be prolonged by sympathetic nerve stimulation. We are currently examining the membrane potential stabilizing effects of leaky K channels at the cellular level.
We have also identified a novel molecule that interacts with leaky K channels. To generate CKO of this molecule, we obtained floxed and Cre mice. This CKO is expected to indirectly affect the leaky K current, but this has not yet been tested.
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| Free Research Field |
生理学
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| Academic Significance and Societal Importance of the Research Achievements |
本研究は心房筋の膜電位の安定に、心室筋細胞とは違う機構が存在する可能性を示唆している。心室筋では強力に膜電位を固定している内向き整流性K電流があるが、心房筋ではこの電流は比較的小さい。一方で、リークK電流を活性化すると不整脈が抑制され、ノックアウトすると不整脈が増える事実は、心臓生理学に新しい知見をもたらす可能性がある。また、上室性不整脈に対するリークK電流の影響は明らかなため、病態生理学的、あるいは新規抗不整脈薬の開拓にも意義があるものと思われる。
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