2022 Fiscal Year Final Research Report
Elucidation of pathophysiological mechanism of chronic obstructive pulmonary disease (COPD)-related osteoporosis
| Project/Area Number |
19K18513
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 56020:Orthopedics-related
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| Research Institution | University of Occupational and Environmental Health, Japan |
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Principal Investigator |
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| Project Period (FY) |
2019-04-01 – 2023-03-31
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| Keywords | 慢性閉塞肺疾患 / COPD / 骨粗鬆症 / サルコペニア / モデル動物 / 酸化ストレス / p38 MAPK / ミトコンドリア |
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| Outline of Final Research Achievements |
To elucidate the molecular mechanism of osteoporosis associated with chronic obstructive pulmonary disease (COPD), we conducted investigations using an animal model. In COPD mice, despite no decrease in physical activity, musculoskeletal disorders (trabecular bone loss, impaired bone formation, soleus muscle weight loss, each muscle fiber atrophy, type I muscle fiber to type II muscle fiber switching) occurred, and oxidative stress markers were elevated in vivo. Focusing on p38 MAPK signaling pathway, the oxidative stress-related muscle atrophy signaling pathway, administration of antioxidants or p38 inhibitors prevented skeletal muscle disorder observed in COPD mice. Because of the close relationship between sarcopenia and osteoporosis, the results of our study may be the key to unraveling the molecular mechanism of COPD-associated osteoporosis.
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| Free Research Field |
骨粗鬆症
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| Academic Significance and Societal Importance of the Research Achievements |
改正高年齢者雇用安定法により勤労者は65歳まで継続して働くことが可能となり、高年齢の勤労者における健康寿命の維持・増進は今後の重要なテーマであると言える。慢性閉塞性肺疾患（COPD）は男性骨粗鬆症の主な原因であるが、COPD骨粗鬆症の病態メカニズムは未だ明らかではない。COPD骨粗鬆症の病態機序を解明していくことで、COPDを有する勤労者の健康寿命の維持・増進に貢献できるのではないかと考え、本研究を立案した。近年、勤労者の転倒災害が問題となっており、勤労者における転倒や骨折リスクを軽減させることで、労働力の維持・向上に繋がることが期待され、本研究成果による社会への波及効果は高いと考える。
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