Activated platelets and atherosclerosis

Abstract

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.

Keywords::

• atherosclerosis
• chemokines
• cytokines
• inflammation
• platelets

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.

Notes

ENA-78: Epithelial cell-derived neutrophil-activating peptide-78; GROa: Growth-related oncogene α; L: Ligand; NAP: Neutrophil-activating petide; PF4: Platelet factor 4; RANTES: Regulated on activation, normal T-cell expressed and secreted; SDF: Stromal-derived factor; TARC: Thymus and activation-regulated chemokine; TNFSF: Tumor necrosis factor superfamily.