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2023 Fiscal Year Final Research Report

Mitochondrial inflammation and its mechanisms in the pathogenesis of chronic pain.

Research Project

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Project/Area Number 20K21635
Research Category

Grant-in-Aid for Challenging Research (Exploratory)

Allocation TypeMulti-year Fund
Review Section Medium-sized Section 55:Surgery of the organs maintaining homeostasis and related fields
Research InstitutionKyoto Prefectural University of Medicine

Principal Investigator

amaya fumimasa  京都府立医科大学, 医学(系)研究科(研究院), 教授 (60347466)

Co-Investigator(Kenkyū-buntansha) 中川 貴之  和歌山県立医科大学, 薬学部, 教授 (30303845)
大橋 憲太郎  岐阜大学, 工学部, 准教授 (50332953)
Project Period (FY) 2020-07-30 – 2024-03-31
KeywordsMitochondria
Outline of Final Research Achievements

Intrathecal administration of the mitochondrial inhibitor antimycin to mice did not result in the development of hyperalgesia. Mitochondrial dysfunction and increased expression of cleaved IL-1beta in neurons were observed in the dorsal root ganglia of a mouse model of neuropathic pain. Similarly, increased expression of cleaved IL-1beta was observed in the mouse plantar incision model, where caspase-1, which cleaves IL-1beta, was also expressed in dorsal root ganglion neurons, and intrathecal administration of a caspase-1 inhibitor attenuated hyperalgesia in the plantar incision model.

Free Research Field

疼痛医学

Academic Significance and Societal Importance of the Research Achievements

ミトコンドリアは正常な神経活動を維持するために重要な細胞内小器官である。ミトコンドリア機能が低下すると、Nod like receptor (NLR)を介して細胞内免疫反応が進行し、慢性疾患を引き起こす原因となる。本研究は、知覚神経におけるミトコンドリア機能不全と炎症性サイトカインIL-1βの活性化が関連すること、IL-1βの活性化が術後痛モデルや神経障害性疼痛モデルにおける痛覚過敏成立に関わることを明らかにした。この成果は神経炎症を標的とした新規治療法開発につながるという点において有意義である。

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Published: 2025-01-30  

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