Integration of metabolic signals at the lysosomes in osteoclasts

2023 Fiscal Year Final Research Report

• Project/Area Number: 22K16426
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 54040:Metabolism and endocrinology-related
• Research Institution: Osaka University
• Principal Investigator: Kimura Tetsuya 大阪大学, 微生物病研究所, 特任助教(常勤) (40792346)
• Project Period (FY): 2022-04-01 – 2024-03-31
• Keywords: 破骨細胞 / リソソーム

Outline of Final Research Achievements

This study investigated the function of the lysosome, an intracellular organelle, in osteoclasts. It is known that the acid secreted by osteoclasts initially degrades minerals, which contribute to bone hardness. Subsequently, the enzyme cathepsin breaks down collagen, the structural basis of bone, leading to bone degradation. While these mechanisms are vital for bone metabolism and maintaining health, they can also contribute to diseases such as osteoporosis. In this study, we focused on the role of intracellular signaling proteins located at the lysosomal membrane, rather than on acids or cathepsins. The signaling pathway at the lysosomal membrane, recently discovered, presents a potential target for developing new drugs to treat osteoporosis.

Free Research Field

代謝免疫学

Academic Significance and Societal Importance of the Research Achievements

我が国の人口の高齢化に伴い、骨粗鬆症の患者が今後増加することが見込まれます。また世界の先進国でも人口の高齢化が進んでいます。特に閉経後の高齢女性では骨粗鬆症のリスクが高くなります。骨折により寝たきりになったり介護が必要になると、患者自身の生活の質を下げ、介護者にも負担となります。骨粗鬆症で骨がもろくなるメカニズムの一つが、破骨細胞による骨吸収(骨が分解されること)です。本研究の成果を応用し、新しい骨粗鬆症治療薬を開発できれば、世界中で骨粗鬆症を治療し、特に高齢者の健康増進と、各国における経済損失の抑制につながります。