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Supports platelet-leukocyte crosstalk in atherogenesis; leaves open whether pathway targeting improves outcomes.
Atherosclerosis is an inflammatory disease. Platelets can "inflame" the vascular wall by various mechanisms and thereby initiate and support the development of atherosclerosis. Platelet interaction with leukocytes, endothelial cells, and circulating progenitor cells triggers autocrine and paracrine activation processes, leading to inflammatory and atherogenic cascades at the vascular wall. This review highlights the molecular key components and pathways used by platelets to trigger and accelerate inflammation at the vascular wall and, thereby, atherosclerosis.
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May et al. (2008) studied this question.
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