Journal
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
Volume 20, Issue 3, Pages 495-505Publisher
AMER SOC NEPHROLOGY
DOI: 10.1681/ASN.2008010009
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Funding
- National Institutes of Health [DK54500, K08 DK073497, 5 P50 DK039255, I-IL70083, DK44757]
- Child Health Research Center Scholar Award [K12 HD043376]
- National Kidney Foundation Post-Doctoral Research Fellowship
- National Kidney Foundation Young Investigator
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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-kappa B 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.
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