| Project/Area Number |
18K08098
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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 53020:Cardiology-related
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| Research Institution | Niigata University |
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Principal Investigator |
HOYANO Makoto 新潟大学, 医歯学総合病院, 助教 (40790283)
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| Co-Investigator(Kenkyū-buntansha) |
南野 徹 新潟大学, 医歯学系, 教授 (90328063)
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| Project Period (FY) |
2018-04-01 – 2023-03-31
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| Project Status |
Completed (Fiscal Year 2022)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2020: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2019: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 肺高血圧症 / 肺高血圧 / 細胞老化 / 老化シグナル |
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| Outline of Final Research Achievements |
We developed a mouse model of hypoxia-induced pulmonary hypertension (PH) and found significant reduction of p53 expression in the lungs.
Our in vitro experiments with metabolomic analyses and the Seahorse XF extracellular flux analyzer indicated that suppression of p53 expression in PASMCs led to upregulation of glycolysis and downregulation of mitochondrial respiration, suggesting a proliferative phenotype resembling that of cancer cells. It was previously shown that systemic genetic depletion of p53 in a murine PH model led to more severe lung manifestations.
Although certain results were reported in experiments using pulmonary hypertensive mice, research using human specimens did not proceed due to difficulties in conducting sufficient research activities as a result of retirement and transfer of the research team.
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| Academic Significance and Societal Importance of the Research Achievements |
肺高血圧症におけるp53の役割について解明を進めることができた。今後、ヒト検体を用いた研究により、肺高血圧の発症・進行の機序を解明し、肺高血圧症の予防・治療法の確立を目指したい。
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