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Comment
. 2014 Jan;11(1):8-10.
doi: 10.1038/cmi.2013.48. Epub 2013 Oct 7.

CD36: linking lipids to the NLRP3 inflammasome, atherogenesis and atherothrombosis

Cécile Oury
Comment

CD36: linking lipids to the NLRP3 inflammasome, atherogenesis and atherothrombosis

Cécile Oury. Cell Mol Immunol. 2014 Jan.
No abstract available

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Figures

Figure 1
Figure 1
Linking hyperlipidemia to inflammation in atherogenesis and atherothrombosis. Uptake of the atherogenic lipid mediator oxLDL by CD36 results in the formation of intracellular cholesterol crystals that cause lysosomal destabilization and NLRP3 activation. oxLDL both primes NLRP3 via an NF-κB-dependent pathway and activates NLRP3. CD36-mediated inflammasome activation provides an early pathogenic pathway that links cholesterol accumulation to the chronic inflammatory process of atherosclerosis. During atherogenesis, activated or injured endothelial cells, leucocytes and platelets release ATP that acts in a paracrine manner to transduce sterile inflammatory signals. Among these signals, P2X7 receptors mediate K+ efflux, leading to NLRP3 activation. Because ATP assembles ASC complexes in oxLDL-treated macrophages, P2X7 receptors and CD36 may cooperate in vivo to activate the NLRP3 inflammasome, contributing to plaque formation. In addition to macrophages, CD36 is expressed on platelets, where it mediates oxLDL-dependent platelet activation and potentially further IL-1β release. P2X7 receptors contribute to PDI TF-dependent thrombosis. Consequently, both CD36 and P2X7 receptors may be involved in atherothrombosis upon plaque rupture. oxLDL, oxidized low-density lipoprotein; PDI, protein disulfide isomerase; TF, tissue factor.
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References

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