| Autor: |
Huilcaman R; Faculty of Health Sciences, University of Talca, Talca 3460000, Chile.; Facultad de Ciencias de la Salud, Escuela de Tecnología Médica, Universidad Bernardo OHiggins, General Gana 1702, Santiago 8370854, Chile., Venturini W; Faculty of Health Sciences, University of Talca, Talca 3460000, Chile.; Center for Medical Research, Medical School, University of Talca, Talca 3460000, Chile., Fuenzalida L; Faculty of Health Sciences, University of Talca, Talca 3460000, Chile., Cayo A; Faculty of Health Sciences, University of Talca, Talca 3460000, Chile.; Center for Medical Research, Medical School, University of Talca, Talca 3460000, Chile., Segovia R; Faculty of Health Sciences, University of Talca, Talca 3460000, Chile.; Center for Medical Research, Medical School, University of Talca, Talca 3460000, Chile., Valenzuela C; Center for Medical Research, Medical School, University of Talca, Talca 3460000, Chile., Brown N; Center for Medical Research, Medical School, University of Talca, Talca 3460000, Chile., Moore-Carrasco R; Faculty of Health Sciences, University of Talca, Talca 3460000, Chile. |
| Abstrakt: |
Platelets play important roles in thrombosis-dependent obstructive cardiovascular diseases. In addition, it has now become evident that platelets also participate in the earliest stages of atherosclerosis, including the genesis of the atherosclerotic lesion. Moreover, while the link between platelet activity and hemostasis has been well established, the role of platelets as modulators of inflammation has only recently been recognized. Thus, through their secretory activities, platelets can chemically attract a diverse repertoire of cells to inflammatory foci. Although monocytes and lymphocytes act as key cells in the progression of an inflammatory event and play a central role in plaque formation and progression, there is also evidence that platelets can traverse the endothelium, and therefore be a direct mediator in the progression of atherosclerotic plaque. This review provides an overview of platelet interactions and regulation in atherosclerosis. |
