Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

45
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...
45
Atherosclerosis III: Management01:26

Atherosclerosis III: Management

26
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...
26
Atherosclerosis II: Clinical Manifestations and Diagnostic Tests01:27

Atherosclerosis II: Clinical Manifestations and Diagnostic Tests

33
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)...
33
Atherosclerosis IV: Nursing Management01:23

Atherosclerosis IV: Nursing Management

43
Nursing management for a patient with arteriosclerosis involves a comprehensive approach focusing on lifestyle modification, disease monitoring, education, and symptomatic care. Here is an overview of effective nursing strategies:Assessment and Monitoring: Initial and ongoing assessments are crucial. Nurses must document the patient's medical history, including any hypertension, diabetes, hyperlipidemia, and other cardiovascular diseases. Assessments also cover family history and lifestyle...
43
Peripheral Artery Disease I: Introduction01:30

Peripheral Artery Disease I: Introduction

27
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...
27
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

28
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...
28

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Hypoxia differentially affects coronary vessel formation during heart development.

Cardiovascular research·2026
Same author

Effect of Polymer Structure on the Thermodynamics of Polyelectrolyte Complex Micelle Formation.

Macromolecules·2026
Same author

Sensing of shear stress in vascular endothelial cells - from physiology to pathology.

Journal of cell science·2026
Same author

Defining the vascular niche of human adipose tissue across metabolic states.

Nature metabolism·2026
Same author

Vascular Endothelial Growth Factor-D Improves Lung Vascular Integrity During Acute Lung Injury.

Circulation research·2026
Same author

Novel cardiovascular metabolic risk factor mechanisms and therapeutic opportunities.

European heart journal·2026

Related Experiment Video

Updated: Aug 30, 2025

Implantation of a Carotid Cuff for Triggering Shear-stress Induced Atherosclerosis in Mice
07:51

Implantation of a Carotid Cuff for Triggering Shear-stress Induced Atherosclerosis in Mice

Published on: January 13, 2012

20.3K

JAG1-NOTCH4 mechanosensing drives atherosclerosis.

Celine Souilhol1,2, Blanca Tardajos Ayllon1, Xiuying Li3

  • 1Department of Infection, Immunity and Cardiovascular Disease, INSIGNEO Institute for In Silico Medicine, and the Bateson Centre, University of Sheffield, Sheffield, UK.

Science Advances
|August 31, 2022
PubMed
Summary
This summary is machine-generated.

Disturbed blood flow activates the JAG1-NOTCH4 pathway in endothelial cells (ECs), promoting atherosclerosis. Targeting this pathway may offer new treatments for this arterial disease.

More Related Videos

Quantification of Atherosclerosis in Mice
06:59

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

38.1K
Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
09:06

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice

Published on: February 20, 2019

8.4K

Related Experiment Videos

Last Updated: Aug 30, 2025

Implantation of a Carotid Cuff for Triggering Shear-stress Induced Atherosclerosis in Mice
07:51

Implantation of a Carotid Cuff for Triggering Shear-stress Induced Atherosclerosis in Mice

Published on: January 13, 2012

20.3K
Quantification of Atherosclerosis in Mice
06:59

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

38.1K
Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
09:06

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice

Published on: February 20, 2019

8.4K

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Cellular Signaling

Background:

  • Endothelial cells (ECs) sense disturbed blood flow, initiating atherosclerosis, a major cause of heart attack and stroke.
  • The Notch pathway is crucial for vascular homeostasis, but its role in flow sensing remains uncharacterized.

Purpose of the Study:

  • To investigate the role of the Notch pathway in endothelial cell sensing of disturbed blood flow.
  • To elucidate the mechanisms by which disturbed flow and Notch signaling contribute to atherosclerosis.

Main Methods:

  • Utilized porcine and murine arteries and human coronary artery ECs.
  • Employed light-sheet imaging and single-cell RNA sequencing.
  • Generated EC-specific Jag1 knockout mice (Jag1ECKO).

Main Results:

  • Disturbed blood flow activates the JAG1-NOTCH4 signaling pathway in ECs.
  • JAG1 and NOTCH4 are enriched in ECs within atherosclerotic plaques.
  • EC-specific deletion of Jag1 reduced atherosclerosis and revealed Jag1's role in suppressing EC proliferation and migration.

Conclusions:

  • JAG1-NOTCH4 signaling in ECs senses disturbed flow, exacerbating atherosclerosis by regulating EC heterogeneity.
  • Targeting the JAG1-NOTCH4 pathway presents a potential therapeutic strategy for atherosclerosis.