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Related Concept Videos

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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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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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...
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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 but also impacts other areas, such as the arms, thereby impairing overall circulation and organ function.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty deposits inside the arterial...
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Atherosclerosis II: Clinical Manifestations and Diagnostic Tests01:27

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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)...
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Related Experiment Video

Updated: Aug 5, 2025

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
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Dendritic cell marker Clec4a4 deficiency limits atherosclerosis progression.

Rossella Bellini1, Annalisa Moregola1, Jasmine Nour1

  • 1Department of Excellence of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Milan, Italy.

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Summary
This summary is machine-generated.

The C-type lectin receptor Clec4a4 (Dendritic cell immunoreceptor 2) promotes atherosclerosis. Its absence in mice reduced plaque formation, altered lipid metabolism, and impaired immune cell distribution, suggesting a pro-atherosclerotic role.

Keywords:
AtherosclerosisC-type lectin receptorsClec4a4Dendritic cellsImmune response

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Area of Science:

  • Immunology
  • Cardiovascular Biology
  • Metabolic Disease

Background:

  • Atherosclerosis pathogenesis involves lipid metabolism and immune responses.
  • Dendritic cells (DCs) are implicated in atherosclerosis, but their specific roles are unclear.
  • Clec4a4 (Dendritic cell immunoreceptor 2) is expressed by CD8α- DCs and modulates T cell immunity.

Purpose of the Study:

  • To investigate the role of Clec4a4 in atherosclerosis.
  • To determine if Clec4a4 deficiency affects atherosclerosis-related immune responses and plaque formation.

Main Methods:

  • Mice lacking Clec4a4 (Dcir2-/-) and Ldlr-/- mice were fed standard or cholesterol-enriched diets for 12 weeks.
  • Immune cell profiles in circulation and lymph nodes were analyzed.
  • Plasma lipid levels and aortic atherosclerotic plaque extent were assessed.

Main Results:

  • Clec4a4 expression decreased under hypercholesterolemia.
  • Clec4a4 deficiency in Ldlr-/- mice reduced atherosclerotic plaque formation.
  • Altered lipid metabolism and impaired myeloid immune cell distribution were observed in Clec4a4-deficient mice.

Conclusions:

  • Clec4a4 plays a pro-atherosclerotic role in experimental models.
  • Targeting Clec4a4 may offer a therapeutic strategy for atherosclerosis.