Our data identify a molecular pathway of thrombosis that involves platelet MRP-14 and CD36 and suggest that targeting MRP-14 has potential for treating atherothrombotic disorders, including MI and stroke.
In recent years, the central activating platelet collagen receptor, glycoprotein (GP) VI, has emerged as a promising antithrombotic target because its blockade or antibody-mediated depletion in circulating platelets was shown to effectively inhibit experimental thrombosis and thromboinflammatory disease states, such as stroke, without affecting hemostatic plug formation.
The double-mutant mice rescued the angiogenic deficit associated with the BDNF(Met/Met) mice without alterations in BDNF levels, indicating that the behavioral deficit in BDNF(Met/Met) mice after stroke is partly related to an unfavorable balance in pro-angiogenic BDNF and anti-angiogenic TSP-1/CD36.
In humans, CD36 variants have been identified to influence free FA and high-density lipoprotein (HDL) levels and to associate with the risk of the metabolic syndrome, coronary artery disease and stroke.
Large epidemiological studies should prove whether the platelet collagen receptor GPIa-IIa T807 allele is an independent risk factor for the development of stroke in younger patients.