Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Sci. Signal., 26 May 2009
Vol. 2, Issue 72, p. re3
[DOI: 10.1126/scisignal.272re3]

REVIEWS

CD36, a Scavenger Receptor Involved in Immunity, Metabolism, Angiogenesis, and Behavior

Roy L. Silverstein* and Maria Febbraio

Department of Cell Biology, Lerner Research Institute, Cleveland Clinic Foundation and Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH 44195, USA.

Gloss: CD36 is a multifunctional cell-surface receptor present on many cell types, including platelets, mononuclear phagocytes, and muscle, fat, and gut cells. It is conserved in mammals, and there are many invertebrate orthologs. CD36 binds to several major classes of ligands, including the matrix protein thrombospondin, long-chain fatty acids, and oxidized phospholipids and lipoproteins; in different contexts, it serves to regulate angiogenesis, innate immune responses, fatty acid metabolism, and sensory responses to fatty acids. CD36 signaling is mediated by activation of specific intracellular pathways that may include kinases of the Src family and mitogen-activated protein kinases. Because of the importance of CD36 signaling in human diseases, including atherosclerosis, thrombosis, Alzheimer’s disease, obesity, diabetes, and cancer, these signaling pathways are under intense scrutiny. This Review includes two figures and 123 citations.

* Corresponding author. E-mail, silverr2{at}ccf.org

Citation: R. L. Silverstein, M. Febbraio, CD36, a Scavenger Receptor Involved in Immunity, Metabolism, Angiogenesis, and Behavior. Sci. Signal. 2, re3 (2009).

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Reduced CD36-dependent tissue sequestration of Plasmodium-infected erythrocytes is detrimental to malaria parasite growth in vivo.
J. Fonager, E. M. Pasini, J. A. M. Braks, O. Klop, J. Ramesar, E. J. Remarque, I. O. C. M. Vroegrijk, S. G. van Duinen, A. W. Thomas, S. M. Khan, et al. (2012)
J. Exp. Med. 209, 93-107
   Abstract »    Full Text »    PDF »
Gene Expression in Livers of BALB/C and C57BL/6J Mice Fed a High-Fat Diet.
S. Nishikawa, J. Sugimoto, M. Okada, T. Sakairi, and S. Takagi (2012)
Toxicol Pathol 40, 71-82
   Abstract »    Full Text »    PDF »
Clinical significance of serum levels of sCD36 in patients with systemic sclerosis: preliminary data.
I. H. Bassyouni, T. A. Gheita, and R. M. Talaat (2011)
Rheumatology 50, 2108-2112
   Abstract »    Full Text »    PDF »
Luminal Lipid Regulates CD36 Levels and Downstream Signaling to Stimulate Chylomicron Synthesis.
T. T. T. Tran, H. Poirier, L. Clement, F. Nassir, M. M. A. L. Pelsers, V. Petit, P. Degrace, M.-C. Monnot, J. F. C. Glatz, N. A. Abumrad, et al. (2011)
J. Biol. Chem. 286, 25201-25210
   Abstract »    Full Text »    PDF »
Platelet CD36 surface expression levels affect functional responses to oxidized LDL and are associated with inheritance of specific genetic polymorphisms.
A. Ghosh, G. Murugesan, K. Chen, L. Zhang, Q. Wang, M. Febbraio, R. M. Anselmo, K. Marchant, J. Barnard, and R. L. Silverstein (2011)
Blood 117, 6355-6366
   Abstract »    Full Text »    PDF »
Lysophosphatidic acid suppresses endothelial cell CD36 expression and promotes angiogenesis via a PKD-1-dependent signaling pathway.
B. Ren, J. Hale, S. Srikanthan, and R. L. Silverstein (2011)
Blood 117, 6036-6045
   Abstract »    Full Text »    PDF »
Vav-Vav-Vav-voom!.
C. J. Lowenstein (2011)
Blood 117, 5557-5559
   Full Text »    PDF »
CD36 Protein Is Involved in Store-operated Calcium Flux, Phospholipase A2 Activation, and Production of Prostaglandin E2.
O. Kuda, C. M. Jenkins, J. R. Skinner, S. H. Moon, X. Su, R. W. Gross, and N. A. Abumrad (2011)
J. Biol. Chem. 286, 17785-17795
   Abstract »    Full Text »    PDF »
Hematopoietic Cell-Restricted Deletion of CD36 Reduces High-Fat Diet-Induced Macrophage Infiltration and Improves Insulin Signaling in Adipose Tissue.
H. T. Nicholls, G. Kowalski, D. J. Kennedy, S. Risis, L. A. Zaffino, N. Watson, P. Kanellakis, M. J. Watt, A. Bobik, A. Bonen, et al. (2011)
Diabetes 60, 1100-1110
   Abstract »    Full Text »    PDF »
Vav Family Rho Guanine Nucleotide Exchange Factors Regulate CD36-mediated Macrophage Foam Cell Formation.
S. O. Rahaman, W. Swat, M. Febbraio, and R. L. Silverstein (2011)
J. Biol. Chem. 286, 7010-7017
   Abstract »    Full Text »    PDF »
αM{beta}2 Integrin Activation Prevents Alternative Activation of Human and Murine Macrophages and Impedes Foam Cell Formation.
V. P. Yakubenko, A. Bhattacharjee, E. Pluskota, and M. K. Cathcart (2011)
Circ. Res. 108, 544-554
   Abstract »    Full Text »    PDF »
Polymorphisms in the CD36/FAT gene are associated with plasma vitamin E concentrations in humans.
S. Lecompte, F. Szabo de Edelenyi, L. Goumidi, G. Maiani, G. Moschonis, K. Widhalm, D. Molnar, A. Kafatos, A. Spinneker, C. Breidenassel, et al. (2011)
Am J Clin Nutr 93, 644-651
   Abstract »    Full Text »    PDF »
CD36: the common soil for inflammation in obesity and atherosclerosis?.
Z. Yang and X.-F. Ming (2011)
Cardiovasc Res 89, 485-486
   Full Text »    PDF »
Brain angiogenesis inhibitor 1 (BAI1) is a pattern recognition receptor that mediates macrophage binding and engulfment of Gram-negative bacteria.
S. Das, K. A. Owen, K. T. Ly, D. Park, S. G. Black, J. M. Wilson, C. D. Sifri, K. S. Ravichandran, P. B. Ernst, and J. E. Casanova (2011)
PNAS 108, 2136-2141
   Abstract »    Full Text »    PDF »
Common CD36 SNPs reduce protein expression and may contribute to a protective atherogenic profile.
L. Love-Gregory, R. Sherva, T. Schappe, J.-S. Qi, J. McCrea, S. Klein, M. A. Connelly, and N. A. Abumrad (2011)
Hum. Mol. Genet. 20, 193-201
   Abstract »    Full Text »    PDF »
Nuclear Orphan Receptor TAK1/TR4-Deficient Mice Are Protected Against Obesity-Linked Inflammation, Hepatic Steatosis, and Insulin Resistance.
H. S. Kang, K. Okamoto, Y.-S. Kim, Y. Takeda, C. D. Bortner, H. Dang, T. Wada, W. Xie, X.-P. Yang, G. Liao, et al. (2011)
Diabetes 60, 177-188
   Abstract »    Full Text »    PDF »
The Evolution of Extracellular Matrix.
S. Ozbek, P. G. Balasubramanian, R. Chiquet-Ehrismann, R. P. Tucker, and J. C. Adams (2010)
Mol. Biol. Cell 21, 4300-4305
   Abstract »    Full Text »    PDF »
Oxidized Low-Density Lipoprotein and Atherosclerosis.
D. Steinberg and J. L. Witztum (2010)
Arterioscler Thromb Vasc Biol 30, 2311-2316
   Full Text »    PDF »
Regulation of Platelet Function by Class B Scavenger Receptors in Hyperlipidemia.
A. Zimman and E. A. Podrez (2010)
Arterioscler Thromb Vasc Biol 30, 2350-2356
   Abstract »    Full Text »    PDF »
Tlr2 is critical for diet-induced metabolic syndrome in a murine model.
R. W. Himes and C. W. Smith (2010)
FASEB J 24, 731-739
   Abstract »    Full Text »    PDF »
Disease-causing mutations within the lysosomal integral membrane protein type 2 (LIMP-2) reveal the nature of binding to its ligand {beta}-glucocerebrosidase.
J. Blanz, J. Groth, C. Zachos, C. Wehling, P. Saftig, and M. Schwake (2010)
Hum. Mol. Genet. 19, 563-572
   Abstract »    Full Text »    PDF »

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882