Analysis of crosstalk mechanisms of cellular responses in chronic diseases

2021 Fiscal Year Final Research Report

• Project/Area Number: 19H03824
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Review Section: Basic Section 57020:Oral pathobiological science-related
• Research Institution: Osaka University
• Principal Investigator: Murakami Tomohiko 大阪大学, 歯学研究科, 講師 (50510723)
• Project Period (FY): 2019-04-01 – 2022-03-31
• Keywords: 炎症 / 小胞体ストレス

Outline of Final Research Achievements

This study found that endoplasmic reticulum stress does not induce an inflammatory response alone, but rather has the effect of enhancing that response during an inflammatory response. As a result of this enhanced inflammatory response, ER stress promotes the expression of inflammatory cytokines such as IL-6. The results of this study suggest that chronic inflammation in endoplasmic reticulum stress-related diseases is related to the enhancement of the inflammatory response by endoplasmic reticulum stress, and that endoplasmic reticulum stress may be involved in the development of chronic inflammation.

Free Research Field

分子細胞生物学

Academic Significance and Societal Importance of the Research Achievements

小胞体ストレスと慢性炎症の相互作用機序とその役割の解明は、関連する疾患の発症機構および生体制御の理解につながり、新しい細胞応答の概念構築に結びつくと考えられる。特に不明な点が多い炎症の慢性化メカニズムにも小胞体ストレスによる炎症増強効果が関与する可能性が示唆される。さらに、この作用機序を阻害することで、小胞体ストレスおよび慢性炎症関連疾患に対する新規治療戦略に応用できる可能性がある。