ArticleThe Journal of clinical investigation2011
Nicotinic acid inhibits progression of atherosclerosis in mice through its receptor GPR109A expressed by immune cells.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.
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Who cites it
125 citing papers in PubMed, 265 citations in OpenAlex.
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- Acute reduction of lipolysis reduces adiponectin and IL-18: evidence from an intervention study with acipimox and insulin.Diabetologia · 2013Trial
- Niacin and biosynthesis of PGD₂by platelet COX-1 in mice and humans.The Journal of clinical investigation · 2012 · on this mapTrial
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- Obesity-derived metabolites modulate anti-tumor immunity in the tumor microenvironment: from mechanisms to clinical applications.BMC medicine · 2026Review
- A new type of biomarker for heat stress: insights from immunology.Frontiers in immunology · 2026Review
- Hydroxycarboxylic acid receptor 2 (GPR109A) and retinopathies: pathways and prospects.Frontiers in medicine · 2026Review
- GPR41 deficiency alters the gut microbiota-bile acid axis, reduces ileal expression ofGut microbes · 2025Article
- Fumarate Signaling in Cardiovascular Disease: Therapeutic Potential and Pathologic Pitfalls of DMF/MMF and FH1 Deficiency.Journal of cardiovascular translational research · 2025Review
- HCAR2 is a novel receptor for heme.Blood advances · 2025Article
- The hydroxycarboxylic acid receptor HCA2 is required for the protective effect of ketogenic diet in epilepsy.Pharmacology research & perspectives · 2024Article
- NADCell communication and signaling : CCS · 2024Review
- Role of Gut Microbial Metabolites in Cardiovascular Diseases-Current Insights and the Road Ahead.International journal of molecular sciences · 2024Review
- High-density lipoprotein in diabetes: Structural and functional relevance.Journal of diabetes investigation · 2024Review
- GPCR Screening Reveals that the Metabolite Receptor HCAR3 Regulates Epithelial Proliferation, Migration, and Cellular Respiration.The Journal of investigative dermatology · 2024Article
- Article
- α-methyltryptophan-mediated protection against diabetic nephropathy inFrontiers in pharmacology · 2024Article
- Molecular Mechanisms of Neuroprotection by Ketone Bodies and Ketogenic Diet in Cerebral Ischemia and Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- Structural insights into ligand recognition and selectivity of the human hydroxycarboxylic acid receptor HCAR2.Cell discovery · 2023Article
65 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nicotinic acid (niacin) is a drug used to reduce the progression of atherosclerosis. Its antiatherosclerotic activity is believed to result from lipid-modifying effects, including its ability to decrease LDL cholesterol and increase HDL cholesterol levels in plasma. Here, we report that in a mouse model of atherosclerosis, we found that nicotinic acid inhibited disease progression under conditions that left total cholesterol and HDL cholesterol plasma levels unaffected. The antiatherosclerotic effect was not seen in mice lacking the receptor for nicotinic acid GPR109A. Surprisingly, transplantation of bone marrow from GPR109A-deficient mice into atherosclerosis-prone animals also abrogated the beneficial effect of nicotinic acid. We detected expression of GPR109A in macrophages in atherosclerotic plaques. In macrophages from WT mice, but not from GPR109A-deficient animals, nicotinic acid induced expression of the cholesterol transporter ABCG1 and promoted cholesterol efflux. Furthermore, activation of GPR109A by nicotinic acid inhibited MCP-1-induced recruitment of macrophages into the peritoneal cavity and impaired macrophage recruitment to atherosclerotic plaques. In contrast with current models, our data show that nicotinic acid can reduce the progression of atherosclerosis independently of its lipid-modifying effects through the activation of GPR109A on immune cells. We conclude therefore that GPR109A mediates antiinflammatory effects, which may be useful for treating atherosclerosis and other diseases.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.