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KAKEN_18K07423seika.pdf
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サルコペニアの新規分子機構の解明と治療戦略の創出
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サルコペニア ノ シンキ ブンシ キコウ ノ カイメイ ト チリョウ センリャク ノ ソウシュツ
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Sarukopenia no shinki bunshi kikō no kaimei to chiryō senryaku no sōshutsu
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Elucidation of novel molecular mechanism of sarcopenia
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遠藤, 仁
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エンドウ, ジン
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Endō, Jin
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慶應義塾大学・医学部 (信濃町) ・講師
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Research team head
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科研費研究者番号 : 50398608
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2021
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科学研究費補助金研究成果報告書
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2020
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加齢性骨格筋萎縮の予防は健康寿命の伸長のために重要です。我々は、従来、血圧調節分子として知られていたプロレニン受容体PRRが、老化と関連が深いWnt-βカテニンシグナルやYAPシグナルを活性化することで加齢性骨格筋萎縮の病態形成に関与することを明らかにしました。PRR-Wntシグナルの活性化は、筋線維の早熟分化を誘導し、筋芽細胞の融合を阻害することで、結果的に筋線維、特に速筋線維の萎縮を起こします。PRR中和抗体、Wnt阻害薬、YAP阻害薬はそれぞれ筋萎縮を抑制する効果を示し、加齢性骨格筋萎縮の治療薬になる可能性を示しました。
Prevention of age-related skeletal muscle atrophy, so called sarcopenia, is important for extending healthy life expectancy. We revealed that the prorenin receptor PRR, which was conventionally known as a blood pressure regulator, was involved in the pathogenesis of sarcopenia by activating Wnt-β-catenin signaling , which are closely related to aging, and YAP signaling. Activation of the PRR-Wnt signaling axis induced premature differentiation of muscle cells to inhibit myoblast fusion, resulting in the atrophy of muscle fibers, especially fast fibers. PRR-neutralizing antibodies, Wnt inhibitors, and YAP inhibitors each exhibited the effect of restoring muscle atrophy, and showed the potential to be a therapeutic drug for sarcopenia.
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研究種目 : 基盤研究 (C) (一般)
研究期間 : 2018~2020
課題番号 : 18K07423
研究分野 : 循環器内科学
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