Braunersreuther V, Mach F
Cardiology Division, Department of Medicine, Geneva University Hospital, Foundation for Medical Research, 64 Avenue Roseraie, 1211 Geneva, Switzerland.
Cell Mol Life Sci. 2006 Sep;63(18):2079-88. doi: 10.1007/s00018-006-6127-2.
Atherosclerosis is a complex inflammatory disease involving cellular migration and interaction. Vascular injury in response to different cardiovascular risk factors enhances endothelial dysfunction, which in turn promotes the expression of inflammatory markers and transendothelial leukocyte migration. Recruitment of leukocytes from the blood stream into the vessel intima is a crucial step for the development of the disease. Recent findings have highlighted the role of chemokines, chemokine receptors, adhesion molecules, and gap junctions in this process by acting as chemoattractant, adhesive, or intercellular communication molecules. In this short review, we summarize new data concerning the different steps from leukocyte arrest to transendothelial migration and discuss potential new therapeutic approaches concerning these processes.
动脉粥样硬化是一种涉及细胞迁移和相互作用的复杂炎症性疾病。对不同心血管危险因素的血管损伤会加剧内皮功能障碍,进而促进炎症标志物的表达和跨内皮白细胞迁移。白细胞从血流中募集到血管内膜是该疾病发展的关键步骤。最近的研究结果突出了趋化因子、趋化因子受体、黏附分子和缝隙连接在这一过程中的作用,它们分别作为化学引诱剂、黏附分子或细胞间通讯分子发挥作用。在这篇简短的综述中,我们总结了有关白细胞停滞到跨内皮迁移不同步骤的新数据,并讨论了针对这些过程的潜在新治疗方法。