The cardioprotective role of the G protein-coupled receptor FFAR4 in atherosclerosis is independent of macrophage foam cell regulation. J Biol Chem 2025 May;301(5):108463
Date
03/30/2025Pubmed ID
40157537Pubmed Central ID
PMC12147181DOI
10.1016/j.jbc.2025.108463Scopus ID
2-s2.0-105003141604 (requires institutional sign-in at Scopus site)Abstract
Free fatty acid receptor 4 (FFAR4), also known as G protein-coupled receptor 120, is a long-chain unsaturated fatty acid receptor expressed in multiple tissue types including macrophages. Activation of FFAR4 maintains metabolic homeostasis by regulating adipogenesis, insulin sensitivity, and inflammation. While FFAR4 is best known for its protective role in obesity and diabetes, recent studies have demonstrated that FFAR4 may also prevent the development of atherosclerosis and cardiovascular disease. Given FFAR4's importance in anti-inflammatory signaling in macrophages, we used peritoneal macrophages from WT and FFAR4 KO (Ffar4-/-) mice to test the hypothesis that FFAR4 prevents the development of macrophage foam cell formation. Our data suggest that neither activation of FFAR4 nor deficiency of FFAR4 has any influence on foam cell outcome in oxidized low-density lipoprotein-treated macrophages. These data suggest that FFAR4's cardioprotective roles in atherosclerosis are independent of the regulation of macrophage foam cell formation.
Author List
Stuttgen GM, Ring CJ, Guda VS, Valdivia Esparza GK, Sahoo DAuthor
Daisy Sahoo PhD Dean, Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsAtherosclerosis
Foam Cells
Lipoproteins, LDL
Macrophages, Peritoneal
Mice
Mice, Inbred C57BL
Mice, Knockout
Receptors, G-Protein-Coupled
