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2023 Fiscal Year Final Research Report

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

Research Project

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Project/Area Number 20H03672
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Review Section Basic Section 53020:Cardiology-related
Research InstitutionThe University of Tokyo

Principal Investigator

FUJIU KATSUHITO  東京大学, 医学部附属病院, 特任教授 (30422306)

Co-Investigator(Kenkyū-buntansha) 小島 敏弥  東京大学, 医学部附属病院, 病院診療医(出向) (30625588)
眞鍋 一郎  千葉大学, 大学院医学研究院, 教授 (70359628)
荷見 映理子  東京大学, 医学部附属病院, 特任助教 (70599547)
中山 幸輝  東京大学, 医学部附属病院, 助教 (70721885)
Project Period (FY) 2020-04-01 – 2023-03-31
Keywords心不全 / 心臓突然死 / マクロファージ / 臓器間連携
Outline of Final Research Achievements

This research aims to elucidate the mechanisms by which stress on the heart imprints stress memory onto hematopoietic stem cells through inter-organ communication. In studies using animal models of heart failure, we found that stress from the heart, when examined using parabiosis, does not imprint stress memory through humoral factors. This led us to identify that the phenomenon occurs through neural pathways. Further examination of the bone marrow revealed that neuropathy in the sympathetic nerves occurs. Specifically, although the nerves themselves persist, there is a reduced expression of enzymes that synthesize neurotransmitters. Consequently, we identified that the decrease in active TGF beta within the bone marrow is the inter-organ communication mechanism that accumulates stress in hematopoietic stem cells.

Free Research Field

内科学

Academic Significance and Societal Importance of the Research Achievements

心不全は再発しやすいことが知られているが、その機序は不明であった。本研究では一度心不全を生じた際にそのストレスが造血幹細胞に蓄積する機序を詳細に解析したものである。今回解明した機序に対する治療法の開発によって、心不全の再発を抑制できる可能性がある。心不全の反復は心不全のための入院が増えるだけでなく、他の臓器の病気にもなりやすくなることが知られており、心不全とその併存疾患を同時に抑制することで医療費抑制に貢献できる可能性がある。

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Published: 2025-01-30  

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