Elucidation of the pathogenesis of cardiovascular diseases by stress memory through interorgan cooperation

2019 Fiscal Year Final Research Report

• Project/Area Number: 17H04171
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Cardiovascular medicine
• Research Institution: The University of Tokyo
• Principal Investigator: Fujiu Katsuhito 東京大学, 医学部附属病院, 特任准教授 (30422306)
• Co-Investigator(Kenkyū-buntansha): 眞鍋 一郎 千葉大学, 大学院医学研究院, 教授 (70359628)
• Project Period (FY): 2017-04-01 – 2020-03-31
• Keywords: 心不全 / 心臓マクロファージ / 臓器間連携

Outline of Final Research Achievements

In this study, it was clarified that there is a system to correct homeostasis of the heart when a pressure load is newly applied to the heart by cooperation of the heart, brain and kidney. When mice were created in which this homeostatic mechanism does not function, they developed heart failure and died. Therefore, this new homeostatic mechanism is likely to be associated with the development of heart failure.
Furthermore, as a new cooperation between organs, we discovered the cooperation of the heart, brain, and organ X. In this organ X, a response to the stress on the heart is being performed, and this reaction changed the response to the stress of the heart. This suggested that organ X was also involved in the development of heart failure.

Free Research Field

循環器病学

Academic Significance and Societal Importance of the Research Achievements

心臓の中には実際に心臓を動かす心筋細胞以外に複数の細胞が存在しています。その中で心臓の全細胞の約１％程度しか存在しない、心臓マクロファージというマイナーな細胞に注目して研究を行いました。その結果、この心臓マクロファージが心臓全体の機能をコントロールしていることを発見しました。マクロファージからはアンフィレギュリンというたんぱく質が分泌されます。このたんぱく質は心筋細胞に働き心筋細胞の働きを強くし、心臓への負担に耐えられるようにしていることを見つけました。このたんぱく質を働かせなくしたマウスも心臓に少しでも負担がかかると心臓病になってしまいます。このたんぱく質は治療に応用できる可能性があります。