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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...
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...
Inflammation01:38

Inflammation

Overview
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)...
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...

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Related Experiment Video

Updated: Jun 24, 2026

Single Nuclei Isolation from Coronary Endarterectomy Tissue of Coronary Artery Bypass Graft Patients
09:09

Single Nuclei Isolation from Coronary Endarterectomy Tissue of Coronary Artery Bypass Graft Patients

Published on: April 3, 2026

Transcriptome Sequencing Identified Hub Pathogenic Chemokines In Atherosclerotic Plaques.

Zhongchen Li1, Peijian Wang2, Junchen Si1

  • 1Department of Neurosurgery, Liaocheng People's Hospital.

Journal of Visualized Experiments : Jove
|June 22, 2026
PubMed
Summary
This summary is machine-generated.

Atherosclerotic plaque involves significant transcriptomic changes, with CCL3, CCL4, and CXCL1 identified as key inflammatory factors. This study reveals altered immune cell composition in atherosclerotic plaque, suggesting new therapeutic targets.

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 24, 2026

Single Nuclei Isolation from Coronary Endarterectomy Tissue of Coronary Artery Bypass Graft Patients
09:09

Single Nuclei Isolation from Coronary Endarterectomy Tissue of Coronary Artery Bypass Graft Patients

Published on: April 3, 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
  • Immunology
  • Transcriptomics

Background:

  • Atherosclerotic plaque (AP) is an inflammatory disease of artery walls, often leading to blood flow obstruction.
  • Current anti-inflammatory therapies for AP have limited success, necessitating deeper understanding of its molecular mechanisms.
  • Inflammation plays a critical role in the pathogenesis of atherosclerotic plaque.

Purpose of the Study:

  • To analyze inflammatory factor-related transcriptomic changes in atherosclerotic plaque (AP) using RNA-sequencing (RNA-seq).
  • To identify key genes and pathways involved in AP pathogenesis.
  • To investigate the immune cell infiltration patterns within AP.

Main Methods:

  • RNA-sequencing (RNA-seq) was performed on samples from AP patients (n=11) and controls (n=3).
  • Differential gene expression analysis (DEGs) was conducted using Metascape.
  • KEGG pathway enrichment, immune infiltration (CIBERSORT), and protein-protein interaction (PPI) network analyses were performed.

Main Results:

  • A total of 3713 differentially expressed genes (DEGs) were identified in AP, enriched in immune and inflammation pathways.
  • CCL3, CCL4, and CXCL1 were identified as major hub genes in the AP pathological process.
  • AP exhibited increased M0 macrophages and decreased CD8+ T cells, activated NK cells, and resting mast cells.

Conclusions:

  • CCL3, CCL4, and CXCL1 show differential expression in AP and are associated with altered immune cell composition.
  • These chemokines represent potential targets for future mechanistic studies and therapeutic interventions in atherosclerotic plaque.
  • The study highlights a distinct immune microenvironment within atherosclerotic plaque.