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2022 Fiscal Year Final Research Report

Pathophysiological analysis of vascular calcification

Research Project

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Project/Area Number 20K08875
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 54040:Metabolism and endocrinology-related
Research InstitutionKawasaki Medical School

Principal Investigator

Fujita Shunichi  川崎医科大学, 医学部, 講師 (30722607)

Co-Investigator(Kenkyū-buntansha) 向井 知之  川崎医科大学, 医学部, 教授 (00454421)
内田 治仁  岡山大学, 医歯薬学総合研究科, 教授 (00550857)
小畑 淳史  川崎医科大学, 医学部, 特任研究員 (10771298)
守田 吉孝  川崎医科大学, 医学部, 教授 (50346441)
金藤 秀明  川崎医科大学, 医学部, 教授 (80448034)
Project Period (FY) 2020-04-01 – 2023-03-31
Keywords血管石灰化 / 炎症性サイトカイン / 大動脈 / IL-17A / 慢性炎症
Outline of Final Research Achievements

Aortic culture experiments were performed to evaluate the effects of inflammatory cytokines on vascular calcification. Aortas were excised from mice and cultured in calcification-inducing medium; IL-1β, IL-6, and IL-17A were added, and their effects on calcification were evaluated by micro-CT and tissue staining. The results showed that IL-17A promoted calcification of the aorta in a concentration-dependent manner; IL-1β and IL-6 also showed some promotion tendency, but the difference was not statistically significant.
The results of this study may explain the mechanism of increased risk of vascular complications in patients with psoriasis and psoriatic arthritis. In addition, this model is a relatively simple model for inducing vascular calcification, and we believe it can be applied to the evaluation of candidate drugs for treatment.

Free Research Field

炎症

Academic Significance and Societal Importance of the Research Achievements

本研究成果は、IL-17Aが血管石灰化の促進に働くことを示している。乾癬および乾癬性関節炎は、その病態にIL-17Aが強く関与することが知られている。本研究成果は、乾癬及び乾癬性関節炎患者において血管合併症リスクが増えることの機序の説明になると考える。また、本モデルは比較的簡便に血管石灰化を誘導できるモデルであり、本モデルを用いて治療候補薬剤の評価などにも用いることが出来ると考える。

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Published: 2024-01-30  

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