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血小板セロトニン加重 ニュートロフィール退化による心筋不全/再注血損傷
Maximilian Mauler1,2,3, Nadine Herr2,3, Claudia Schoenichen2,3
1Faculty of Biology (M.M., K.K.), University of Freiburg, Germany.
Circulation
|December 28, 2018
まとめ
血小板セロトニンは再注射傷害後の炎症と心臓損傷を助長します セロトニンの抑制は,中性粒子の活性化を低下させることで,心臓発作の合併症の治療のための新しい治療戦略を提供することができる.
科学分野:
- 心血管科学
- 血液学
- 免疫学
背景:
- 血小板はセロトニンを貯蔵し放出します 血静と炎症に不可欠です
- 心筋再注射損傷および関連する血栓炎症におけるセロトニンの役割は完全に理解されていません.
研究 の 目的:
- 血小板に由来するセロトニンが心筋再注射損傷における役割を調査する.
- 心臓発作後の ニュートロフィール依存性炎症を緩和する 治療目標として セロトニンを研究する
主な方法:
- 血小板セロトニンの遺伝的および薬学的減少による心筋再注射損傷のマウスモデルを使用した.
- ヒトとマウスの血小板と白血球で in vitro セロトニン刺激アッセイを行った.
- 急性冠動脈症候群の患者およびマウスにおける血セロトニン,中性粒子の活性化マーカーCD11b,およびミエロペロキシダースの測定
主要な成果:
- 血小板セロトニンは中性粒子の脱粒化を誘発し,炎症を増加させ,マウスの心臓組織を回復させました.
- 急性冠動脈症候群患者における血セロトニンの上昇は中性粒子のCD11bとミエロペロキシダース値と相関する.
- セロトニンの再吸収抑制により,血小板セロトニンが減少し,中性粒子の活性化が低下し,マウスおよび患者の心臓機能が保たれた.
結論:
- セロトニンは,心筋再注射損傷における中性粒子の誘発性血栓炎症の主要な媒介である.
- セロトニンを標的とする治療は 心臓発作の合併症の管理に 有望な治療法です
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