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

2.0K
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...
2.0K
Atherosclerosis III: Management01:26

Atherosclerosis III: Management

589
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...
589
Atherosclerosis IV: Nursing Management01:23

Atherosclerosis IV: Nursing Management

574
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...
574
Atherosclerosis II: Clinical Manifestations and Diagnostic Tests01:27

Atherosclerosis II: Clinical Manifestations and Diagnostic Tests

754
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)...
754
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

992
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...
992
Coronary Artery Disease I: Introduction01:30

Coronary Artery Disease I: Introduction

1.6K
Coronary Artery Disease (CAD): An Overview with Scientific InsightsCoronary Artery Disease (CAD), often referred to as C-A-D, is a prevalent blood vessel disorder classified under the broader category of atherosclerosis. Atherosclerosis is a pathological process characterized by the hardening and narrowing of arteries due to the accumulation of atherosclerotic plaques. These plaques are composed of cholesterol, fatty substances, inflammatory cells, calcium, and fibrin, reducing blood flow to...
1.6K

You might also read

Related Articles

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

Sort by
Same author

Deficiency of antioxidant enzyme PRDX6 and mucosal chemokine CXCL17: unraveling the factors behind oxidative stress and mucosal homeostasis disruption in dry eye disease.

Biochimica et biophysica acta. Molecular basis of disease·2025
Same author

Characterization of the Orphan Cytochrome P450 CYP135B1 from <i>Mycobacterium tuberculosis</i>: Involvement in Metabolism but Not in the Antibacterial Activity of the Antitubercular Drug SQ109.

ACS infectious diseases·2025
Same author

Antagonistic actions of PAK1 and NF2/Merlin drive myelin membrane expansion in oligodendrocytes.

Glia·2024
Same author

Expanded biochemical analyses of human tear fluid: Polyvalent faces of the schirmer strip.

Experimental eye research·2023
Same author

Profiling tear film enzymes reveals major metabolic pathways involved in the homeostasis of the ocular surface.

Scientific reports·2023
Same author

Identification of the specific molecular and functional signatures of pre-beta-HDL: relevance to cardiovascular disease.

Basic research in cardiology·2023

Related Experiment Video

Updated: Apr 4, 2026

Aggravation of Myocardial Ischemia upon Particulate Matter Exposure in Atherosclerosis Animal Model
07:35

Aggravation of Myocardial Ischemia upon Particulate Matter Exposure in Atherosclerosis Animal Model

Published on: December 10, 2021

2.5K

SASH1, a new potential link between smoking and atherosclerosis.

Henri Weidmann1, Zahia Touat-Hamici2, Herve Durand2

  • 1Sorbonne Universités, UPMC, UMR_S 1166-ICAN, Genomics and Pathophysiology of Cardiovascular Diseases, Institute of Cardiometabolism and Nutrition, ICAN, Pitié-Salpêtrière Hospital, F-75013, Paris, France; University Heart Center Hamburg, Clinic for General and Interventional Cardiology, Hamburg, Germany; German Center for Cardiovascular Research (DZHK e.V.) Partner Site Hamburg, Lübeck, Kiel, Hamburg, Germany.

Atherosclerosis
|August 31, 2015
PubMed
Summary

Smoking increases SASH1 expression in carotid atherosclerosis. Silencing SASH1 in endothelial cells enhances cell migration, proliferation, and angiogenesis, linking smoking to atherosclerosis via SASH1.

Keywords:
AtherosclerosisCCND1CCND3SASH1SmokingTP53

More Related Videos

Quantification of Atherosclerosis in Mice
06:59

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

41.1K
Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus
06:43

Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus

Published on: December 7, 2013

14.8K

Related Experiment Videos

Last Updated: Apr 4, 2026

Aggravation of Myocardial Ischemia upon Particulate Matter Exposure in Atherosclerosis Animal Model
07:35

Aggravation of Myocardial Ischemia upon Particulate Matter Exposure in Atherosclerosis Animal Model

Published on: December 10, 2021

2.5K
Quantification of Atherosclerosis in Mice
06:59

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

41.1K
Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus
06:43

Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus

Published on: December 7, 2013

14.8K

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • Vascular Cell Biology

Background:

  • Smoking is a major risk factor for atherosclerosis.
  • SASH1 expression is elevated in monocytes of smokers and correlates with carotid plaque burden.
  • The role of SASH1 in the vascular wall and its direct link to smoking-induced atherosclerosis requires further investigation.

Purpose of the Study:

  • To validate the association between smoking, SASH1 expression, and atherosclerosis within the vascular wall.
  • To determine the impact of SASH1 on endothelial cell functions, including migration, proliferation, and angiogenesis.

Main Methods:

  • Analysis of SASH1 expression in human carotid arteries from smokers and non-smokers using gene expression and immunostaining.
  • SASH1 knockdown in human aortic endothelial cells (HAECs) via siRNA.
  • Assessment of HAEC functions (migration, proliferation, angiogenesis) and transcriptomic profiling after SASH1 silencing.

Main Results:

  • SASH1 is expressed in vascular cells and macrophages; its expression is significantly higher in atherosclerotic carotids of smokers.
  • SASH1 knockdown in HAECs led to increased cell migration, proliferation, and angiogenesis.
  • SASH1 silencing decreased CYP1A1 expression, potentially via TP53 inhibition.

Conclusions:

  • SASH1 expression is elevated in the atherosclerotic carotids of smokers.
  • SASH1 silencing impacts endothelial angiogenic functions, suggesting a role in smoking-related atherosclerosis.
  • This study provides a potential molecular link between smoking and atherosclerosis mediated by SASH1.