title: Targeting the fatty acid transport protein CD36, a class B scavenger receptor, in the treatment of renal disease.
abstract: Augmentation of the CD36 pathway, which involves the uptake of several endogenous ligands including free fatty acids and oxidized low-density lipoprotein, contributes to the damage of proximal tubules and podocytes, whereas ablation of CD36 attenuates renal injury. Souza et al. demonstrate that 5A peptide can inhibit CD36 signaling, attenuate chronic kidney disease progression, and ameliorate inflammation and tubulointerstitial fibrosis by reducing the expression of inflammatory cytokines and chemokines, suggesting the therapeutic potential of 5A peptide against CD36-mediated renal injury.
authors.affiliation: Department of Nephrology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
authors.forename: Hideki
authors.initials: H
authors.lastname: Yokoi
authors.affiliation: Department of Nephrology, Kyoto University Graduate School of Medicine, Kyoto, Japan. Electronic address: motoy@kuhp.kyoto-u.ac.jp.
authors.forename: Motoko
authors.initials: M
authors.lastname: Yanagita
mesh_terms: D018955:CD36 Antigens; D050612:Fatty Acid Transport Proteins; D006801:Humans; D007674:Kidney Diseases; D008077:Lipoproteins, LDL; D050199:Podocytes / Q000378:metabolism; D051116:Receptors, Scavenger / Q000378:metabolism
chemical_list: D018955:CD36 Antigens; D050612:Fatty Acid Transport Proteins; D008077:Lipoproteins, LDL; D051116:Receptors, Scavenger