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Related Concept Videos

Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

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...
Inflammation01:38

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Sympathetic Signaling01:31

Sympathetic Signaling

Sympathetic signaling, a vital part of the autonomic nervous system, plays a crucial role in mobilizing the body's resources in response to stress or emergencies. It involves the transmission of nerve impulses from sympathetic preganglionic fibers to postganglionic fibers. This results in the release of specific neurotransmitters and activation of adrenergic receptors.
Sympathetic preganglionic fibers release the neurotransmitter acetylcholine (ACh) onto the ganglionic neurons in the...
Coronary Artery Disease II: Pathophysiology01:26

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Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
Sympathetic Activation01:16

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The sympathetic division can influence tissues and organs by releasing norepinephrine at peripheral synapses and distributing epinephrine and norepinephrine through the bloodstream. In times of crisis or stress, sympathetic activation occurs, which is regulated by sympathetic centers in the hypothalamus. As a result, sympathetic activation prepares the body for physical exertion, rapid ATP production, and heightened alertness, allowing individuals to respond effectively to challenging or...
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Related Experiment Video

Updated: Jul 2, 2026

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
05:51

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

Published on: May 6, 2014

Sympathetic neurons exacerbate atherosclerosis by modulating macrophage function via the NPY/Y1R axis.

Yubao Fan1, Dairui Li2, Qiumin Chen3

  • 1Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China; Department of Cardiac Surgery, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, China.

Atherosclerosis
|June 30, 2026
PubMed
Summary

Sympathetic nerves accelerate atherosclerosis by promoting inflammatory macrophages via neuropeptide Y receptor Y1 (Y1R) signaling. Targeting this axis may reduce vascular inflammation and stabilize plaques.

Keywords:
AtherosclerosisInflammationNPY/Y1R axisProinflammatory macrophage polarizationSympathetic regulation

Related Experiment Videos

Last Updated: Jul 2, 2026

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
05:51

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

Published on: May 6, 2014

Area of Science:

  • Cardiovascular Biology
  • Neuroimmunology
  • Atherosclerosis Research

Background:

  • Neuroimmune crosstalk is crucial in atherosclerosis.
  • The sympathetic neuron-macrophage axis role in atherosclerosis is not fully understood.

Purpose of the Study:

  • To investigate how sympathetic innervation influences atherosclerosis via macrophage phenotype and function.
  • To explore the neuropeptide Y receptor Y1 (Y1R) axis in this process.

Main Methods:

  • Atherosclerosis was studied in ApoE-/- mice with and without sympathetic denervation on a high-fat diet.
  • Macrophage phenotype, plaque characteristics, and signaling pathways were analyzed.
  • In vitro coculture and in vivo Y1R inhibition (BIBO3304) were employed.

Main Results:

  • Sympathetic denervation reduced atherosclerotic lesion burden and improved plaque stability.
  • Neuropeptide Y/Y1R signaling promoted macrophage polarization to a proinflammatory phenotype.
  • Y1R inhibition decreased atherosclerotic area, necrotic core size, and proinflammatory macrophages, enhancing plaque stability.

Conclusions:

  • Sympathetic signaling accelerates atherosclerosis by promoting proinflammatory macrophage polarization via the NPY/Y1R axis.
  • Targeting sympathetic inputs or Y1R presents a potential therapeutic strategy for vascular inflammation and plaque stabilization.