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2023 Fiscal Year Final Research Report

Protective molecular mechanism of Spi-B in aortic dissection

Research Project

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Project/Area Number 19K17612
Research Category

Grant-in-Aid for Early-Career Scientists

Allocation TypeMulti-year Fund
Review Section Basic Section 53020:Cardiology-related
Research InstitutionWakayama Medical University

Principal Investigator

Taruya Akira  和歌山県立医科大学, 医学部, 助教 (60612942)

Project Period (FY) 2019-04-01 – 2024-03-31
Keywords大動脈解離 / Spi-B / アンギオテンシンⅡ / 高血圧
Outline of Final Research Achievements

In this study, we focused on Spi-B, a transcription factor of the Ets family, and investigated its association with the development of aortic dissection. We established an aortic dissection model using Spi-B knockout (KO) mice by continuous injection of angiotensin II (ANG II), and induced a prestage state of aortic dissection by hypertensive loading with ANG II in both wild-type mice and Spi-B KO mice. Then, histopathological, immunohistochemical, gene expression kinetics, and protein expression kinetics were analyzed. The results showed that Spi-B KO resulted in structural fragility of the aorta. We found that aortic component proteins produced by Spi-B-expressing fibroblasts play a major role in this.

Free Research Field

循環器内科

Academic Significance and Societal Importance of the Research Achievements

大動脈解離は「突然死」の原因となる疾患のひとつである。何らかの原因で大動脈構造の変性が起こり大動脈が脆弱な状態となった結果、血圧上昇を契機に大動脈中膜の解離が生じることで大動脈解離が発症すると考えられている。一方、大動脈構造変性に対する予防法は確立しておらず、大動脈解離を発症して初めて治療が行われているのが現状である。本研究の結果により、Spi-Bが大動脈の構造維持に寄与していることが明らかになった。今後Spi-Bを標的とした新規分子標的治療の礎となると考えられる。

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Published: 2025-01-30  

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