Pericleous C, Giles I, Rahman A
Medical Molecular Biology Unit, Institute of Child Health, University College London, London WC1N 1EH, UK and Centre for Rheumatology Research, Division of Medicine, University College London, London W1T 4JF, UK.
Lupus. 2009 Jul;18(8):671-5. doi: 10.1177/0961203309103062.
Vascular dysfunction is key to the development of thrombosis in the antiphospholipid syndrome. This has been largely demonstrated by the upregulation of various cell surface and intracellular signalling molecules, as well as proinflammatory cytokine release from activated endothelial cells. Endothelial microparticles (EMP) are a further marker of endothelial activation but have been less extensively studied. We summarise evidence suggesting that these microparticles may be critical effectors of thrombosis in the antiphospholipid syndrome. There is evidence that levels of EMP are raised in patients with circulating antiphospholipid antibodies and that these EMP may be prothrombotic. The balance between markers of endothelial dysfunction (including EMP and circulating endothelial cells) and markers of repair such as circulating endothelial progenitor cells may be abnormal in patients with APS but this has not been proved and requires further study.
血管功能障碍是抗磷脂综合征中血栓形成的关键因素。这在很大程度上已通过各种细胞表面和细胞内信号分子的上调以及活化内皮细胞释放促炎细胞因子得到证实。内皮微粒（EMP）是内皮激活的另一个标志物，但研究较少。我们总结了证据表明这些微粒可能是抗磷脂综合征中血栓形成的关键效应物。有证据表明，循环抗磷脂抗体患者的EMP水平升高，且这些EMP可能具有促血栓形成作用。在抗磷脂综合征患者中，内皮功能障碍标志物（包括EMP和循环内皮细胞）与修复标志物（如循环内皮祖细胞）之间的平衡可能异常，但这尚未得到证实，需要进一步研究。
