GPR109A and Vascular Inflammation

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 “pleiotropi...

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Bibliographic Details
Published in:Current atherosclerosis reports 2013-05, Vol.15 (5), p.325-325, Article 325
Main Authors: Chai, Joshua T., Digby, Janet E., Choudhury, Robin P.
Format: Article
Language:English
Subjects:
Angiology
Arrestins - physiology
Atherosclerosis - drug therapy
Atherosclerosis - immunology
Atherosclerosis - physiopathology
Cardiology
Humans
Hypolipidemic Agents - therapeutic use
Lipoproteins - metabolism
Medicine
Medicine & Public Health
Niacin - therapeutic use
Receptors, G-Protein-Coupled - agonists
Receptors, G-Protein-Coupled - immunology
Receptors, G-Protein-Coupled - physiology
Receptors, Nicotinic - immunology
Receptors, Nicotinic - physiology
Section Editor
Topical Collection on Vascular Biology
Vascular Biology (RS Rosenson
Vascular Biology (RS Rosenson, Section Editor)
Vasculitis - drug therapy
Vasculitis - immunology
Vasculitis - physiopathology
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Summary: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 β-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.
ISSN:1523-3804
1534-6242
DOI:10.1007/s11883-013-0325-9