Schematic representation demonstrating that the activation of platelets elicits a thromboinflammatory response that is manifested by the release of cytokines, leukocyte activation, and the formation of platelet-leukocyte aggregates. These factors contribute to the pathogenesis of CVD, including myocardial infarction. The activation of platelet CXCR7 alters the platelet lipidome and generates lipid species that inhibit the thromboinflammatory function of platelets, thus affording protection from thrombosis and myocardial infarction. IFN-γ, interferon-γ; TGF-β, transforming growth factor-β; TNF-α, tumor necrosis factor-α. Figure created with BioRender.com.

Schematic representation demonstrating that the activation of platelets elicits a thromboinflammatory response that is manifested by the release of cytokines, leukocyte activation, and the formation of platelet-leukocyte aggregates. These factors contribute to the pathogenesis of CVD, including myocardial infarction. The activation of platelet CXCR7 alters the platelet lipidome and generates lipid species that inhibit the thromboinflammatory function of platelets, thus affording protection from thrombosis and myocardial infarction. IFN-γ, interferon-γ; TGF-β, transforming growth factor-β; TNF-α, tumor necrosis factor-α. Figure created with BioRender.com.

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