2023 Fiscal Year Final Research Report
Elucidation of Novel Pathogenic Mechanisms and Molecular Functional Analysis in Sudden Cardiac Death and Heart Failure
Project/Area Number |
20K08466
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 53020:Cardiology-related
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Research Institution | The University of Tokyo |
Principal Investigator |
Hasumi Eriko 東京大学, 医学部附属病院, 特任助教 (70599547)
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Co-Investigator(Kenkyū-buntansha) |
藤生 克仁 東京大学, 医学部附属病院, 特任准教授 (30422306)
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Project Period (FY) |
2020-04-01 – 2024-03-31
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Keywords | S100A8 / 肥満 / 糖尿病 / マクロファージ / 慢性炎症 / 突然死 / 心室細動 / 脂肪組織 |
Outline of Final Research Achievements |
Recent studies have revealed that chronic inflammation and fibrosis in cardiac tissue are causes of arrhythmia. Particularly, findings have been reported suggesting that inflammation of adipose tissue around the heart and systemic inflammation could be factors in the development of arrhythmias. Additionally, our research has shown that S100A8 is expressed not only in adipose tissue but also in the cardiovascular system, kidneys, lungs, and liver, and that it induces inflammation in these organs. Based on these results, this study will investigate the possibility that chronic inflammation induced by S100A8 signaling in the cardiovascular system and inflammation in various organs are interrelated and contribute to arrhythmias such as atrial fibrillation and ventricular fibrillation.
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Free Research Field |
循環器内科、予防医学
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Academic Significance and Societal Importance of the Research Achievements |
近年の臨床研究において、肥満が心不全発症や、心房細動といった不整脈発症に関連していると報告がされており、基礎研究では局所臓器での炎症が心不全や心房細動発症の原因となっていることも報告されるようになってきている。しかし、いまだ詳細な機序や多臓器との相関については明らかとなっていない。そこで、S100A8のシグナルを介した、心臓への影響を解明することで、心不全や不整脈の発症機序解明に非常に有用である。このような研究の報告は今までになく、特にS100A8が上昇する肥満と心疾患に関連を解析する本研究は新規性が高く、将来的に不整脈領域における新規治療法や創薬が実現すれば、社会的意義は非常に高い。
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