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Review
. 2001 Sep;108(6):785-91.
doi: 10.1172/JCI14006.

CD36: a class B scavenger receptor involved in angiogenesis, atherosclerosis, inflammation, and lipid metabolism

M Febbraio  1 , D P Hajjar, R L Silverstein
Affiliations
Review

CD36: a class B scavenger receptor involved in angiogenesis, atherosclerosis, inflammation, and lipid metabolism

M Febbraio et al. J Clin Invest. 2001 Sep.
No abstract available

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Figures

Figure 1
Figure 1
Antagonism of proangiogenic responses by CD36. In response to ligand engagement, a proangiogenic receptor (such as the VEGF or bFGF receptor) induces proliferation, migration, and tube formation of microvascular endothelial cells. In the presence of TSP-1, which interacts with a specific motif (CLESH) on its receptor, CD36, this response is inhibited. Inhibition is mediated through interaction with fyn, the activation of p38 MAP kinase, and, ultimately, caspase DNA cleavage, resulting in endothelial cell apoptosis.
Figure 2
Figure 2
CD36-mediated macrophage foam cell formation. In response to EC injury, macrophages and LDL transmigrate into the subendothelial space (I), where they may become entrapped. Inflammatory stimuli (II) lead to the secretion of oxidative products from ECs and macrophages, including nitric oxide (NO), hydrogen peroxide, and myeloperoxidase (MPO) (III), which act upon LDL particles and convert them into CD36-specific ligands, or ligands for other scavenger receptors (SR). Internalization of oxidized LDL via CD36 (IV) generates lipid byproducts (e.g., 9-HODE, 13-HODE, and PGJ2), mediated by lipoxygenase or other pathways, which in turn provide ligands for the transcription factor PPARγ (V). The binding of these lipids structurally enables PPARγ to dimerize with binding partners such as RXR and charges the complex for nuclear translocation and the activation of transcription of target genes (VI). Because these target genes include both PPARγ and CD36, a positive feedback loop arises. The increased expression of CD36 promotes further oxidized LDL uptake, perpetuating the cycle and resulting in accumulation of cholesterol ester by macrophages and eventually in foam cell formation (VII). Adapted from ref. .
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