Silverstein Roy L
Department of Cell Biology, Lerner Research Institute, Cleveland Clinic Foundation, Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, 9500 Euclid Ave 44195, NC10, Cleveland, OH, USA Tel.: +1 216 444 5220.
Clin Lipidol. 2009 Dec;4(6):767. doi: 10.2217/clp.09.57.
Platelet hyper-reactivity and a systemic prothrombotic state are associated with atherosclerosis and other inflammatory conditions. CD36, a member of the Type 2 scavenger receptor family, is a multiligand pattern recognition receptor that recognizes specific oxidized phospholipids, molecules expressed on microbial pathogens, apoptotic cells, and cell-derived microparticles. Recent studies have demonstrated that CD36 binding to oxidized LDL or microparticles activates a specific signaling pathway that induces platelet activation. This pathway is activated in vivo in the setting of hyperlipidemia and oxidant stress. Genetic deletion of CD36 protects mice from pathological thrombosis associated with hyperlipidemia without any apparent effect on normal hemostasis. Targeting CD36 or its signaling pathway could potentially lead to the development of novel antithrombotic therapies for patients with atheroinflammatory disorders.
血小板高反应性和全身性血栓前状态与动脉粥样硬化及其他炎症性疾病相关。CD36是2型清道夫受体家族的成员，是一种多配体模式识别受体，可识别特定的氧化磷脂、微生物病原体上表达的分子、凋亡细胞和细胞衍生的微粒。最近的研究表明，CD36与氧化型低密度脂蛋白或微粒的结合会激活一条诱导血小板活化的特定信号通路。在高脂血症和氧化应激情况下，该通路在体内被激活。CD36基因缺失可保护小鼠免受与高脂血症相关的病理性血栓形成，而对正常止血无明显影响。靶向CD36或其信号通路可能会为动脉粥样硬化性炎症疾病患者开发新的抗血栓治疗方法。
