Examination of the significance of CD206-positive M2 macrophages in the pathogenesis of obese cardiomyopathy

2019 Fiscal Year Final Research Report

• Project/Area Number: 19K21300
• Project/Area Number (Other): 18H06195 (2018)
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Multi-year Fund (2019); Single-year Grants (2018)
• Review Section: 0902:General internal medicine and related fields
• Research Institution: University of Toyama
• Principal Investigator: Liu Jianhui 富山大学, 学術研究部医学系, 特命助教 (80828640)
• Project Period (FY): 2018-08-24 – 2020-03-31
• Keywords: マクロファージ / 心不全 / 心筋症

Outline of Final Research Achievements

The purpose of this study is to investigate the significance of CD206-positive M2 macrophages in the pathogenesis of obese cardiomyopathy. In conclusion, it is suggested that M2 macrophages have a protective effect on hypervascularization in adipose tissue in the early stage of obesity cardiomyopathy and interstitial hyperfibrosis in the heart, which is the terminal image of obesity cardiomyopathy. In addition, it protects against myocardial hypertrophy that results from increased interstitial fibrosis in the heart, which is a phenotype of obese cardiomyopathy, and heart failure, which is its terminal image, through the regulation of sarcomere genes and fibrosis-related genes, and has a protective effect. It was strongly suggested that it could be a promising therapeutic target for the treatment of heart failure.

Free Research Field

内科学

Academic Significance and Societal Importance of the Research Achievements

M2マクロファージは肥満心筋症の病初期の脂肪組織における血管増生と肥満心筋症の終末像である心臓での間質繊維化亢進に対し保護的に作用することが示唆された。肥満心筋症の表現型である心臓での間質繊維化亢進の結果で生じる心筋肥大およびその終末像である心不全に対し、サルコメア遺伝子と線維化関連遺伝子の制御に通じて、保護的に作用し心不全治療の有望な治療標的になりうることが強く示唆された。本研究を通して学術的には “局所マクロファージ機能不全関連疾患”の概念が確立され、循環器医学・生物学に貢献するとともに社会的には局所マクロファージを標的にした治療の可能性が生まれ、臨床医学の発展に寄与することが期待される。