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CD36 Regulates Oxidative Stress and Inflammation in Hypercholesterolemic CKD

By Daryl M. Okamura, Subramaniam Pennathur, Katie Pasichnyk, Jesús M. López-Guisa, Sarah Collins, Maria Febbraio, Jay Heinecke and Allison A. Eddy

Abstract

Scavenger receptors play a central role in atherosclerosis by processing oxidized lipoproteins and mediating their cellular effects. Recent studies suggested that the atherogenic state correlates with progression of chronic kidney disease (CKD); therefore, scavenger receptors are candidate mediators of renal fibrogenesis. Here, we investigated the role of CD36, a class B scavenger receptor, in a hypercholesterolemic model of CKD. We placed CD36-deficient mice and wild-type male mice on a high-fat Western diet for 7 to 8 wk and then performed either sham or unilateral ureteral obstruction surgery. CD36-deficient mice developed significantly less fibrosis compared with wild-type mice at days 3, 7, and 14 after obstruction. Compared with wild-type mice, CD36-deficient mice had significantly more interstitial macrophages at 7 d but not at 14 d. CD36-deficient mice exhibited reduced levels of activated NF-κB and oxidative stress (assessed by measuring fatty acid–derived hydroxyoctadecadienoic acid and protein carbonyl content) and decreased accumulation of interstitial myofibroblasts compared with wild-type mice. These data suggest that CD36 is a key modulator of proinflammatory and oxidative pathways that promote fibrogenesis in CKD

Topics: Basic Research
Publisher: American Society of Nephrology
OAI identifier: oai:pubmedcentral.nih.gov:2653683
Provided by: PubMed Central
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