Targeting Platelet in Atherosclerosis Plaque Formation: Current Knowledge and Future Perspectives

Figures

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  Figure 1. Disturbed flow-regulated platelets participate in the plaque formation. Disturbed flow activates endothelial cells (ECs), resulting in elevated expression of adhesion molecules and deposition of adhesion proteins. All these adhesion molecules and proteins interact with platelets via surface receptors, leading to platelet activation. Activated platelets recruit circulating leukocytes by P-selectin or other releasing inflammatory factors, therefore participating atherogenesis.

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  Figure 2. Platelets participate in atherosclerosis under hyperlipidemic conditions. Lipoproteins, such as low-density lipoproteins in plasma, trigger platelet activation by binding sites. Or monocytes engulf low-density lipoprotein (LDL)-containing apoptotic platelets and migrate under the inner membrane to differentiate into macrophages and foam cells. Subendothelial oxidized LDL further participates in atherosclerotic plaque formation by binding to scavenger receptor CD36 and LOX-1.

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  Figure 3. As an inflammatory mediator, platelets interact with ECs and leukocytes (mainly monocytes) to participate in the formation of atherosclerotic lesions. Pro-atherosclerosis factors can easily lead to platelet activation. The activated platelets express a variety of adhesion receptors. These receptors bind their matrix proteins (GPIb-vWF, GPVI-collagen, and GPIIb-IIIa-fibrinogen) to mediate platelet adhesion on ECs or leukocytes (P-selectin-PSGL-1 and Clec2-PDPN). Moreover, platelet activation releases a variety of inflammatory factors (cytokines, chemokines, growth factors, and others). These inflammatory mediators can also be induced and expressed in neighboring cells, such as monocytes/macrophages, neutrophils, and ECs, which in turn affected platelets. Blue arrow: the factor released by platelets interact with leukocytes; Black solid arrow: the rolling of leukocytes; Blue dotted arrow: activated leukocytes in turn affect platelets.