Over the past decade, platelets have been demonstrated to have various functions beyond their role in hemostasis.
Platelets possess a rich repertoire of chemokines that are stored in their alpha granules and can be released upon activation.
The pro-atherogenic effects of activated platelets are most likely mediated by release of these pro-inflammatory
mediators that promote recruitment, activation or differentiation of other cell types including endothelial cells and leukocytes.
These effects have been excellently reviewed in the past by various authors. The current review will therefore focus
on novel findings. A specific focus will be put on CXCL4, on which a lot of new data have been published since 2008.
Thus, the effects of CXCL4 on macrophage differentiation have been studied in detail revealing that CXCL4 induces a
specific macrophage phenotype. Furthermore, novel data on CXCL4L1, a protein similar to CXCL4 that is probably transcribed
from a duplication of the PF4 gene coding for CXCL4, will be discussed. A very interesting study has recently
demonstrated that the inhibition of heterophilic chemokine interactions using a specifically designed small molecule can
inhibit atherogenesis in Apoe-/- mice, thereby demonstrating the clinical potential of tackling platelet chemokines as therapeutic
targets in atherosclerosis. Finally, novel data on CXCL1 and CCL5 will be discussed. Overall, while our understanding
of the role of platelet chemokines in atherogenesis has significantly improved over the past years, it seems that
there may still be many buried treasures in this field that could improve disease prevention or lead to novel clinical therapies.
Keywords: Platelets, chemokines, chemokine receptors, atherogenesis, atherosclerosis, signal transduction, pro-inflammatory mediators, leukocytes, monocytes, acute myocardial infarction
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