Platelet CD36 links hyperlipidemia, oxidant stress and a prothrombotic phenotype

@article{Podrez2007PlateletCL,
  title={Platelet CD36 links hyperlipidemia, oxidant stress and a prothrombotic phenotype},
  author={Eugene A. Podrez and Tatiana V. Byzova and Maria Febbraio and Robert G. Salomon and Yi Ma and Manojkumar Valiyaveettil and Eugenia Poliakov and Mingjiang Sun and Paula J Finton and Brian R. Curtis and Juhua Chen and Renliang Zhang and Roy L. Silverstein and Stanley L. Hazen},
  journal={Nature Medicine},
  year={2007},
  volume={13},
  pages={1086-1095}
}
Dyslipidemia is associated with a prothrombotic phenotype; however, the mechanisms responsible for enhanced platelet reactivity remain unclear. Proatherosclerotic lipid abnormalities are associated with both enhanced oxidant stress and the generation of biologically active oxidized lipids, including potential ligands for the scavenger receptor CD36, a major platelet glycoprotein. Using multiple mouse in vivo thrombosis models, we now demonstrate that genetic deletion of Cd36 protects mice from… 
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  • Biology, Medicine
    Arteriosclerosis, thrombosis, and vascular biology
  • 2010
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It is demonstrated that platelet class B scavenger receptors play roles in thrombosis in dyslipidemia and may contribute to acute cardiovascular events in vivo in hypercholesterolemia.
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References

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TLDR
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TLDR
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TLDR
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TLDR
The biology of CD36 can be broadly divided in terms of functions that it mediates with or without TSP-1, but it is probable that it acts in concert with other proteins, such as fatty acid–binding proteins, caveola-associated proteins, integrins, cytoskeletal proteins, and signaling molecules, to effect its diverse functions.
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TLDR
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