Aukrust Pål, Halvorsen Bente, Ueland Thor, Michelsen Annika E, Skjelland Mona, Gullestad Lars, Yndestad Arne, Otterdal Kari
Research Institute for Internal Medicine, Oslo University Hospital Rikshospitalet, N-0027 Oslo, Norway.
Expert Rev Cardiovasc Ther. 2010 Sep;8(9):1297-307. doi: 10.1586/erc.10.92.
Several studies suggest an important role for platelets in atherogenesis, not only as mediators of thrombus formation, but also as inducers of inflammation. Several lines of evidence indicate that platelets are potent inflammatory cells that induce inflammatory responses in adjacent cells such as leukocytes and endothelial cells. Platelets may also themselves respond to inflammatory mediators produced by these neighboring cells. These platelet-mediated inflammatory pathways contribute to atherogenesis in both the early and late stage of the process. The bidirectional interaction between platelets and other cells may also be involved in the nonresolving inflammation characterizing atherosclerosis. In patients with atherosclerotic disorders, platelet-mediated inflammation appears to be operating in spite of the wide use of platelet-inhibiting drugs. This underscores the need for new therapeutic tools that more specifically target the pathways in platelet-mediated inflammation.
多项研究表明，血小板在动脉粥样硬化形成过程中发挥着重要作用，不仅作为血栓形成的介质，还作为炎症诱导剂。多条证据表明，血小板是强大的炎症细胞，可诱导相邻细胞如白细胞和内皮细胞产生炎症反应。血小板自身也可能对这些邻近细胞产生的炎症介质作出反应。这些血小板介导的炎症途径在动脉粥样硬化形成的早期和晚期阶段均起作用。血小板与其他细胞之间的双向相互作用也可能参与了动脉粥样硬化所特有的持续性炎症。在患有动脉粥样硬化疾病的患者中，尽管广泛使用了血小板抑制药物，但血小板介导的炎症似乎仍在发生。这突出表明需要有更特异性地靶向血小板介导炎症途径的新治疗工具。
