Journal
CURRENT ATHEROSCLEROSIS REPORTS
Volume 15, Issue 5, Pages -Publisher
CURRENT MEDICINE GROUP
DOI: 10.1007/s11883-013-0325-9
Keywords
GPR109A; HCA(2); HM74a; Niacin; Nicotinic acid; beta-arrestin; Macrophage; Lipoproteins; Atherosclerosis; Inflammation
Categories
Funding
- BHF Centre of Research Excellence, Oxford
- Oxford Comprehensive Biomedical Research Centre NIHR
- Medical Research Council [MR/K00266X/1] Funding Source: researchfish
- MRC [MR/K00266X/1] Funding Source: UKRI
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GPR109A has generated expanding interest since its discovery as the receptor for niacin a decade ago, along with deorphanisation as the receptor for endogenous ligand 3-hydroxy-butyrate shortly after. This interest is generated especially because of the continuing exploration of niacin's pleiotropic mechanisms of action and its potential in the cross-talk between metabolic and inflammatory pathways. As GPR109A's primary pharmacological ligand in clinical use, niacin has been used for over 50 years in the treatment of cardiovascular disease, mainly due to its favourable effects on plasma lipoproteins. However, it has become apparent that niacin also possesses lipoprotein-independent effects that influence inflammatory pathways mediated through GPR109A. In addition to its G-protein-mediated effects, recent evidence has emerged to support alternative GPR109A signalling via adaptive protein beta-arrestins. In this article, we consider the role of GPR109A and its downstream effects in the context of atherosclerosis and vascular inflammation, along with insights into strategy for future drug development.
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