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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

Inflammation

Overview
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

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...
Peripheral Artery Disease I: Introduction01:30

Peripheral Artery Disease I: Introduction

Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs, particularly the arteries supplying the thighs and calves. In rare cases, it may involve other arteries, including those in the arms.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty...
Atherosclerosis II: Clinical Manifestations and Diagnostic Tests01:27

Atherosclerosis II: Clinical Manifestations and Diagnostic Tests

Atherosclerosis is a progressive disorder that leads to the thickening and narrowing of arterial walls due to plaque buildup. This condition can cause various symptoms depending on the arteries affected:Coronary Artery Disease (CAD): This condition affects the coronary arteries and may lead to chest pain (angina), shortness of breath (dyspnea), heart attacks, and other heart disease symptoms.Cerebrovascular Disease: This affects blood flow to the brain, causing transient ischemic attacks (TIAs)...
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...

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Related Experiment Video

Updated: Jun 19, 2026

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
09:41

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions

Published on: October 17, 2017

Atherosclerosis progression and monocyte emigration from plaque.

René Rs Packard1, Guo-Ping Shi

  • 1Cardiovascular Medicine, Brigham & Women's Hospital, Harvard Medical School, NRB-742, 77 Avenue Louis Pasteur, Boston. rpackard@rics.bwh.harvard.edu

Future Cardiology
|October 7, 2009
PubMed
Summary

Monocyte emigration from atherosclerotic plaques is reduced during disease progression. This impaired cell removal, driven by mediators like platelet-activating factor, may worsen inflammation in atherosclerosis.

More Related Videos

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

Related Experiment Videos

Last Updated: Jun 19, 2026

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
09:41

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions

Published on: October 17, 2017

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
  • Immunology
  • Atherosclerosis Research

Background:

  • Monocytes/macrophages are key immune cells in atherosclerotic lesions.
  • Understanding monocyte fate in atherosclerosis is crucial for disease management.
  • Dyslipidemia's impact on monocyte behavior within plaques requires investigation.

Purpose of the Study:

  • To investigate how dyslipidemia influences the emigration of monocytes from atherosclerotic plaques.
  • To determine if monocyte emigration differs between progressive and regressive atherosclerotic lesions.
  • To explore the mechanisms hindering monocyte egress from developing plaques.

Main Methods:

  • Utilized an in vitro model of the vessel wall to assess monocyte emigration.
  • Employed an in vivo aortic arch transplantation model in mice.
  • Analyzed monocyte-derived cell emigration into plaque-draining lymph nodes.

Main Results:

  • Platelet-activating factor and lysophosphatidic acid impair monocyte emigration from cultured vessel walls.
  • In vivo studies showed reduced emigration of monocyte-derived cells during atherosclerotic lesion progression.
  • Atherosclerosis progression is linked to decreased monocyte emigration and increased recruitment.

Conclusions:

  • Reduced emigration of monocyte-derived cells is a hallmark of progressive atherosclerosis.
  • Impaired monocyte egress, alongside recruitment, contributes to plaque accumulation.
  • Sequestered cells may exhibit dendritic cell-like features, potentially exacerbating local inflammation.