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PCSK9 (プロプロテインコンバーターゼ サブチリシン/ケキシン9) 血小板活性化,血栓形成,心筋梗塞拡張を強める
Zhiyong Qi1, Liang Hu2, Jianjun Zhang3
1Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, China (Z.Q., W.Y., D.J., Z.Y., K.Y., A.S., J.Q., J.G.).
Circulation
|September 29, 2020
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PubMed で要約を見る
まとめ
プロプロテインコンバーターゼサブチリシン/ケキシン9 (PCSK9) は,CD36に結合することで,血小板活性化と血栓形成を直接促進する. アスピリンとPCSK9阻害剤はこれらの血栓性合併症を予防できるので,高リスクの患者には併用療法が推奨されます.
科学分野:
- 心血管生物学
- 血液学
- 分子医学
背景:
- プロプロテイン変換酵素サブチリシン/ケキシン9 (PCSK9) は,主に低密度リポプロテイン受容体を分解することによって,血低密度リポプロテインコレステロールを調節する.
- PCSK9は脂質代謝以外にもプレオトロピ的効果があることが知られているが,血小板活性化と血栓形成に対する直接的な影響はほとんど特徴づけられていない.
研究 の 目的:
- PCSK9が血小板活性化,凝結,血栓形成に及ぼす直接的な影響を調査する.
- PCSK9が血小板機能に影響を与える基本的な分子メカニズムを解明する.
- PCSK9が心筋梗塞 (MI) の膨張と小血管阻害における役割を評価する.
主な方法:
- PCSK9の血小板集積,濃い粒子のATP放出,インテグリンαIIbβ3活性化,α-粒子の放出,拡散,凝固の収縮に対するインビトロ効果を評価した.
- FeCl3が誘発したマウス中枢動脈栓塞のモデルを使用して,体内の血栓塞の評価を行った.
- CD36,Srcキナーゼ,MAPKシグナル伝達,活性酸素種,およびトロンボキサンA2を含むメカニズム的経路を調査した.
- 心筋梗塞 (MI) モデルにおけるPCSK9の役割を調べ,マイクロ血管阻害と心臓梗塞の拡大を評価した.
主要な成果:
結論:
- プラズマPCSK9は,CD36媒介のシグナル伝達により,血小板活性化,in vivo血栓形成,およびMI後の拡張を直接強化する.
- PCSK9阻害剤とアスピリンはこれらの血栓抑制効果を効果的に軽減します.
- アスピリンとPCSK9阻害剤を併用した治療は,PCSK9濃度が上昇した患者の血栓性合併症の予防に有益である可能性があります.