A novel mechanism to regulate chronic inflammation through metabolic remodeling in obesity and senescence

2019 Fiscal Year Final Research Report

• Project/Area Number: 17K08879
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Immunology
• Research Institution: Mie University
• Principal Investigator: OGATA Masato 三重大学, 医学系研究科, 教授 (60224094)
• Co-Investigator(Kenkyū-buntansha): 竹林 慎一郎 三重大学, 生物資源学研究科, 准教授 (50392022) ; 大隈 貞嗣 三重大学, 医学系研究科, 助教 (70444429)
• Project Period (FY): 2017-04-01 – 2020-03-31
• Keywords: 慢性炎症 / 代謝症候群 / 細胞老化 / MAPキナーゼ / エピゲノム

Outline of Final Research Achievements

It is well established that the chronic inflammation is implicated in many diseases such as metabolic syndrome and cancer. However, the precise mechanism of the chronic inflammation has not been clarified yet. We have found that the chronic inflammation signaling cascade is involved in the development of type I diabetes and the accelerated aging in mouse models. Furthermore, we have demonstrated that the senescence of cells results in the metabolic remodeling which can induce the epigenetic modifications of proinflammatory cytokine genes and thus, can affect the senescence-associated secretory phenotype.

Free Research Field

免疫学

Academic Significance and Societal Importance of the Research Achievements

慢性炎症は多くの疾患と関わることから、それを生じる機構の解明は病態の理解や治療に欠かせない。本研究結果は、細胞老化によって生じる代謝リモデリングから遺伝子発現変化に至る分子機構を明らかにすることで、生活習慣病やがんの促進因子の理解と制御に役立つ。また、エピゲノム解析の目的で開発した新手法は、これまで困難であった単細胞での網羅的なゲノム構造変化を解析でき、本研究のみならず遺伝子の構造制御機構の解明にも有用である。