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Related Concept Videos

Atherosclerosis III: Management01:26

Atherosclerosis III: Management

Management of atherosclerosis involves an integrated strategy encompassing pharmacological treatment, surgical interventions, lifestyle changes, and nutrition therapy to address the multifactorial nature of the disease.Pharmacological TherapyA cornerstone of atherosclerosis management is the use of pharmacological agents. Statins, such as atorvastatin, are pivotal in inhibiting HMG-CoA reductase, an enzyme that catalyzes an initial step in cholesterol synthesis in the liver. This reduction in...
Atherosclerosis I: Introduction01:30

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Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
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Drugs Acting on Autonomic Ganglia: Blockers01:28

Drugs Acting on Autonomic Ganglia: Blockers

Ganglionic blockers inhibit autonomic activity by blocking nicotinic receptors in the autonomic ganglia, suppressing impulse transmission. These blockers lack selectivity between sympathetic and parasympathetic ganglia and are ineffective as neuromuscular junction antagonists. They can be categorized into two groups:
Cholinergic Receptors: Nicotinic01:15

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Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating sympathetic or...

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Related Experiment Video

Updated: Jun 4, 2026

Quantification of Atherosclerosis in Mice
06:59

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

Nicotinic acid inhibits progression of atherosclerosis in mice through its receptor GPR109A expressed by immune

Martina Lukasova1, Camille Malaval, Andreas Gille

  • 1Department of Pharmacology, Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany.

The Journal of Clinical Investigation
|February 15, 2011
PubMed
Summary
This summary is machine-generated.

Nicotinic acid (niacin) reduces atherosclerosis progression by activating the GPR109A receptor on immune cells, independent of its lipid-modifying effects. This mechanism offers new therapeutic strategies for inflammatory diseases.

Related Experiment Videos

Last Updated: Jun 4, 2026

Quantification of Atherosclerosis in Mice
06:59

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

Area of Science:

  • Cardiovascular Research
  • Immunology
  • Pharmacology

Background:

  • Nicotinic acid (niacin) is known to reduce atherosclerosis progression, primarily attributed to its lipid-modifying effects.
  • These effects include decreasing LDL cholesterol and increasing HDL cholesterol levels.

Purpose of the Study:

  • To investigate the antiatherosclerotic mechanism of nicotinic acid beyond its lipid-modifying properties.
  • To determine the role of the nicotinic acid receptor GPR109A in mediating these effects.

Main Methods:

  • Utilized a mouse model of atherosclerosis.
  • Investigated the effects of nicotinic acid in wild-type and GPR109A-deficient mice and bone marrow chimeras.
  • Analyzed GPR109A expression in macrophages within atherosclerotic plaques.
  • Assessed cholesterol transporter ABCG1 expression and cholesterol efflux in macrophages.
  • Evaluated the impact of nicotinic acid on macrophage recruitment.

Main Results:

  • Nicotinic acid inhibited atherosclerosis progression even when plasma lipid levels remained unchanged.
  • The antiatherosclerotic effect was abolished in mice lacking GPR109A and in bone marrow chimeras lacking GPR109A.
  • GPR109A was expressed in macrophages within atherosclerotic plaques.
  • Nicotinic acid-activated GPR109A induced ABCG1 expression and cholesterol efflux in macrophages.
  • Nicotinic acid inhibited MCP-1-induced macrophage recruitment and plaque infiltration.

Conclusions:

  • Nicotinic acid reduces atherosclerosis progression via GPR109A activation on immune cells, independent of lipid modification.
  • GPR109A activation mediates anti-inflammatory effects, including reduced macrophage recruitment.
  • GPR109A-mediated anti-inflammatory actions present a novel therapeutic target for atherosclerosis and other inflammatory conditions.