Format

Send to

Choose Destination
Nat Rev Nephrol. 2017 Dec;13(12):769-781. doi: 10.1038/nrneph.2017.126. Epub 2017 Sep 18.

CD36 in chronic kidney disease: novel insights and therapeutic opportunities.

Author information

1
Centre for Nephrology & Urology, Shenzhen University Health Science Center, 3688 Nanhai Avenue, Shenzhen 518060, China.
2
Seattle Children's Research Institute, Center for Developmental Biology & Regenerative Medicine, University of Washington, 1900 9th Avenue, C9S-5, Seattle, Washington 98101, USA.
3
Centre for Lipid Research & Key Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, the Second Affiliated Hospital, Chongqing Medical University, 1 Yixueyuan Road, 400016 Chongqing, China.
4
John Moorhead Laboratory, Centre for Nephrology, University College London, Rowland Hill Street, London NW3 2PF, UK.

Abstract

CD36 (also known as scavenger receptor B2) is a multifunctional receptor that mediates the binding and cellular uptake of long-chain fatty acids, oxidized lipids and phospholipids, advanced oxidation protein products, thrombospondin and advanced glycation end products, and has roles in lipid accumulation, inflammatory signalling, energy reprogramming, apoptosis and kidney fibrosis. Renal CD36 is mainly expressed in tubular epithelial cells, podocytes and mesangial cells, and is markedly upregulated in the setting of chronic kidney disease (CKD). As fatty acids are the preferred energy source for proximal tubule cells, a reduction in fatty acid oxidation in CKD affects kidney lipid metabolism by disrupting the balance between fatty acid synthesis, uptake and consumption. The outcome is intracellular lipid accumulation, which has an important role in the pathogenesis of kidney fibrosis. In experimental models, antagonist blockade or genetic knockout of CD36 prevents kidney injury, suggesting that CD36 could be a novel target for therapy. Here, we discuss the regulation and post-translational modification of CD36, its role in renal pathophysiology and its potential as a biomarker and as a therapeutic target for the prevention of kidney fibrosis.

PMID:
28919632
DOI:
10.1038/nrneph.2017.126
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Nature Publishing Group
Loading ...
Support Center