2021 Fiscal Year Final Research Report
Pathophysiological mechanism for Ca2+ transport regulation in vascular remodeling and its therapeutic application
| Project/Area Number |
19K07132
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 47040:Pharmacology-related
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| Research Institution | Tokushima Bunri University |
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Principal Investigator |
Kita Satomi 徳島文理大学, 薬学部, 教授 (10461500)
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| Co-Investigator(Kenkyū-buntansha) |
太田 紘也 徳島文理大学, 薬学部, 助教 (40638988)
喜多 知 福岡大学, 医学部, 講師 (50797107)
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| Project Period (FY) |
2019-04-01 – 2022-03-31
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| Keywords | Ca輸送制御 / 血管再構築 |
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| Outline of Final Research Achievements |
Vascular dysfunction and remodeling based on endothelial cell injury and vascular smooth muscle cell proliferation/hypercontraction are deeply involved in the onset of vascular diseases such as pulmonary arterial hypertension (PAH) and peripheral arterial disease. Such vascular diseases may be associated with endothelial and arterial Ca2+ handling abnormality, but the detailed molecular mechanisms are still unknown. In this study, we examined the possibility that Na/Ca exchangers participate in endothelial and arterial Ca2+ handling abnormality. Our results suggest that Ca2+ efflux via NCLX contributes to vascular dysfunction and remodeling.
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| Free Research Field |
薬理学
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| Academic Significance and Societal Importance of the Research Achievements |
ミトコンドリアはATPを産生する重要なオルガネラであるとともに、アポトーシスの誘導、活性酸素種（ROS）の生成など、細胞の生死に関わる多彩な機能を担っている。本研究により、ミトコンドリアから細胞質へのCa2+放出が血管新生、血管リモデリングおよび平滑筋収縮に機能的に働くことが示された。本研究により、NCLXの機能異常が血管病の発症に関与する可能性が示されたことから、NCLXが血管病の新たな治療標的として期待される。
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