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KAKEN_15K09271seika.pdf
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慢性腎臓病における血管・弁膜石灰化分子病態ネットワークの解明と治療標的分子探索
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マンセイ ジンゾウビョウ ニ オケル ケッカン・ベンマク セッカイカ ブンシ ビョウタイ ネットワーク ノ カイメイ ト チリョウ ヒョウテキ ブンシ タンサク
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Mansei jinzōbyō ni okeru kekkan benmaku sekkaika bunshi byōtai nettowāku no kaimei to chiryō hyōteki bunshi tansaku
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Studies on molecular pathological network of vascular and valvular calcification in CKD and survey for therapeutic target
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林, 松彦
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ハヤシ, マツヒコ
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Hayashi, Matsuhiko
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慶應義塾大学・医学部(信濃町)・教授
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Research team head
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科研費研究者番号 : 60129608
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吉田, 理
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ヨシダ, タダシ
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Yoshida, Tadashi
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慶應義塾大学・医学部(信濃町)・准教授
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Research team member
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科研費研究者番号 : 00306713
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2018
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科学研究費補助金研究成果報告書
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2017
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慢性腎臓病において, 血管石灰化を生じることが様々な合併症に関与することが知られている。そこで, 動物実験を通してこの機序を解明するために, 慢性腎臓病の状態を再現したマウスで血管石灰化を生じるモデルを作成した。この時, 大動脈の平滑筋細胞が本来の性質を失い, 骨を形作る骨芽細胞様細胞への形質変換を生じていることが分子レベルで示され, 多くの炎症を起こす疾患で重要な役割を果たすNFκBという蛋白が血管特異的に働かなくなるようにしたマウスでは, 血管石灰化が改善することを明らかとした。以上の結果は, NFκB抑制薬が慢性腎臓病で見られる血管石灰化抑制薬として有用である可能性を示唆する極めて重要な知見と言える。
In the patients with chronic kidney diseases (CKD), it is well known that vascular calcification induces various complications. In this study, we developed a mouse model to reveal the mechanisms of vascular calcification.In this model mouse, vascular smooth muscle cells in the aorta were shown to lose its phenotype and gain the characteristics of osteogenic cells in molecular level. In addition, this phenomenon was ameliorated in the mouse which lost NFkB activity (important protein for various inflammatory diseases). From these findings, it is strongly suggested that inhibitor for NFkB will be a good candidate for the prevention of vascular calcification in CKD.
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研究種目 : 基盤研究(C)(一般)
研究期間 : 2015～2017
課題番号 : 15K09271
研究分野 : 腎臓病学
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