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

1.7K
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...
1.7K
Inflammation01:38

Inflammation

63.3K
Overview
63.3K
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

857
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...
857
Peripheral Artery Disease I: Introduction01:30

Peripheral Artery Disease I: Introduction

521
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...
521
Atherosclerosis II: Clinical Manifestations and Diagnostic Tests01:27

Atherosclerosis II: Clinical Manifestations and Diagnostic Tests

677
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)...
677
Atherosclerosis III: Management01:26

Atherosclerosis III: Management

541
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...
541

You might also read

Related Articles

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

Sort by
Same author

Preoperative cardiovascular evaluation in patients with cancer.

Frontiers in cardiovascular medicine·2026
Same author

Interpreting Pulmonary Hypertension Beyond Single Cells.

Arteriosclerosis, thrombosis, and vascular biology·2026
Same author

JSMel: A dataset of 960 song melodies widely shared in contemporary Japan.

Data in brief·2026
Same author

Investigational New Drug-enabling studies in a human vessel-chip: Are we there yet?

Bioengineering & translational medicine·2026
Same author

Pulmonary vein and posterior wall isolation using the circular, multielectrode catheter for treatment of atrial fibrillation: Acute and long-term outcomes from the Pulsed-Field Ablation for PVI Using PulseSelect With Adjunct Posterior Wall Isolation trial.

Heart rhythm·2026
Same author

QT monitoring in chemotherapy.

Frontiers in cardiovascular medicine·2026

Related Experiment Video

Updated: Mar 9, 2026

A Model of Disturbed Flow-Induced Atherosclerosis in Mouse Carotid Artery by Partial Ligation and a Simple Method of RNA Isolation from Carotid Endothelium
11:00

A Model of Disturbed Flow-Induced Atherosclerosis in Mouse Carotid Artery by Partial Ligation and a Simple Method of RNA Isolation from Carotid Endothelium

Published on: June 22, 2010

30.2K

Flow signaling and atherosclerosis.

Nhat-Tu Le1, Uday G Sandhu2, Raymundo A Quintana-Quezada2

  • 1Department of Cardiology, Division of Internal Medicine, The University of Texas MD Anderson Cancer Center, Unit 1101, 1515 Holcombe Blvd., Houston, Texas, 77030-4009, USA. nle3@mdanderson.org.

Cellular and Molecular Life Sciences : CMLS
|January 1, 2017
PubMed
Summary
This summary is machine-generated.

Undisturbed blood flow (u-flow) protects arteries from atherosclerosis, while disturbed flow (d-flow) promotes it. Understanding how these flow patterns affect endothelial cells (ECs) can reveal new ways to combat cardiovascular disease.

Keywords:
AMPKDNA methylationDRP-1ER stressERK5HATs and HDACsMAP kinaseNEMOPKC familyPPARsSENP2SUMOylationp90RSK

More Related Videos

Flow Cytometry Analysis of Immune Cells Within Murine Aortas
15:15

Flow Cytometry Analysis of Immune Cells Within Murine Aortas

Published on: July 1, 2011

35.4K
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

21.2K

Related Experiment Videos

Last Updated: Mar 9, 2026

A Model of Disturbed Flow-Induced Atherosclerosis in Mouse Carotid Artery by Partial Ligation and a Simple Method of RNA Isolation from Carotid Endothelium
11:00

A Model of Disturbed Flow-Induced Atherosclerosis in Mouse Carotid Artery by Partial Ligation and a Simple Method of RNA Isolation from Carotid Endothelium

Published on: June 22, 2010

30.2K
Flow Cytometry Analysis of Immune Cells Within Murine Aortas
15:15

Flow Cytometry Analysis of Immune Cells Within Murine Aortas

Published on: July 1, 2011

35.4K
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

21.2K

Area of Science:

  • Cardiovascular Biology
  • Endothelial Cell Biology
  • Atherosclerosis Research

Background:

  • Atherosclerosis predominantly occurs in arterial regions experiencing disturbed blood flow (d-flow).
  • Undisturbed blood flow (u-flow) is generally considered athero-protective.
  • Differential responses of vascular endothelial cells (ECs) to flow patterns suggest distinct intracellular signaling pathways.

Purpose of the Study:

  • To review molecular events differentially regulated by u-flow and d-flow in ECs.
  • To explore the roles of kinases, ER stress, inflammasome, SUMOylation, and DNA methylation in flow-induced endothelial dysfunction.
  • To understand the interplay of these molecular events in regulating flow-dependent signaling and cellular responses.

Main Methods:

  • Literature review focusing on molecular mechanisms.
  • Analysis of signaling cascades activated by distinct flow patterns in ECs.
  • Discussion of cellular responses leading to endothelial dysfunction and atherosclerosis.

Main Results:

  • u-flow and d-flow activate distinct intracellular signaling cascades in ECs.
  • Kinases, ER stress, inflammasome, SUMOylation, and DNA methylation are key molecular players in differential flow responses.
  • These molecular events interact to regulate flow-dependent signaling and cellular phenotypes.

Conclusions:

  • ECs exhibit distinct molecular responses to u-flow and d-flow.
  • Understanding these differential responses is crucial for developing interventions against endothelial dysfunction and cardiovascular diseases.
  • Targeting specific molecular pathways activated by disturbed flow may offer therapeutic strategies.