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2022 Fiscal Year Final Research Report

A study of the novel molecular mechanism of atrial fibrillation induced by cardiac resident macrophages in hyperuricemia

Research Project

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Project/Area Number 19K08557
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 53020:Cardiology-related
Research InstitutionTottori University

Principal Investigator

TSUNETO Motokazu  鳥取大学, 医学部, 助教 (60730207)

Co-Investigator(Kenkyū-buntansha) 李 佩俐  鳥取大学, 医学(系)研究科(研究院), 助教 (40464292)
久留 一郎  鳥取大学, 医学(系)研究科(研究院), 教授 (60211504)
Project Period (FY) 2019-04-01 – 2023-03-31
Keywords高尿酸血症 / 心臓 / 常在マクロファージ / 心房細動
Outline of Final Research Achievements

Hyperuricemia has been reported to be a risk factor for atrial fibrillation, but the details are unknown. Recently, it has been reported that tissue resident macrophages in the heart associate with the myocardium via gap junctions, and that their disruption causes conduction defects. In this study, we investigated the possibility that hyperuricemia-induced atrial fibrillation is caused by changes in the behavior of cardiac resident macrophages through in vivo mouse models and in vitro analysis, and found that the number of cardiac resident macrophages in hyperuricemia model mice did not change. In addition, the effects of uric acid were examined using human iPS cell-derived pacemaker cells, which showed no electrophysiological effects.

Free Research Field

循環器学

Academic Significance and Societal Importance of the Research Achievements

マウスの心臓常在マクロファージ数は高尿酸状態では変化しなかったため、心房細動とは関係ないことが示唆された。この実験は知りうる限り世界で初めて行われた実験であり、有意義だと思われる。
またマウスの実験は困難であったが、この科学研究費助成事業中にヒトiPS細胞からペースメーカ細胞を誘導する培養法を開発し、論文発表できた。そこで、この細胞を使用して試験管内で尿酸を添加し、パッチクランプ法を用いてヒトiPS細胞由来ペースメーカ細胞イオンチャネルの機能を検討した。尿酸添加群と非添加群でその機能に差は見られなかったが、この実験も世界で初めて行われたものであり、有意義だと思われる。

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Published: 2024-01-30  

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