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.
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Received 15 March 2006; received after revision 19 May 2006; accepted 13 June 2006
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Braunersreuther, V., Mach, F. Leukocyte recruitment in atherosclerosis: Potential targets for therapeutic approaches?. Cell. Mol. Life Sci. 63, 2079–2088 (2006). https://doi.org/10.1007/s00018-006-6127-2
- leukocyte recruitment
- cell adhesion molecule
- gap junction
- therapeutic strategy