Abstract
The CD36 scavenger receptor recognizes oxidized low-density lipoprotein (LDL) and cell-derived microparticles. It is expressed on macrophages and platelets and is a mediator of both atherogenesis and thrombosis. Macrophages from CD36-null mice have a defect in foam cell formation in response to exposure to oxidized LDL, and CD36-null mice fed an atherogenic Western diet have significantly less atherosclerosis than their wild-type counterparts. On platelets, CD36 recognition of oxidized LDL contributes to their activation and provides a mechanistic link between hyperlipidemia, oxidant stress, and the prothrombotic state. Cell-derived microparticles are also major ligands for CD36 and contribute to thrombus formation in a CD36-dependent manner even in the absence of hyperlipidemia. CD36 deficiency in mice is associated with inhibition of thrombus formation and with a reduction in microparticle accumulation in thrombi. Targeting CD36 is a promising avenue for the treatment of atheroinflammatory disorders.