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 Experiment Videos

Cyclooxygenase-2 and atherosclerosis.

MacRae F Linton1, Sergio Fazio

  • 1Department of Medicine, Division of Cardiovascular Medicine, Room 383 PRB, Vanderbilt University Medical Center, Nashville, TN 37232-6303, USA. macrae.linton@mcmail.vanderbilt.edu

Current Opinion in Lipidology
|September 28, 2002
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Interleukin-6 and C-reactive protein prognostic value following acute coronary syndrome.

European heart journal·2026
Same author

Post-transcriptional modifications on tRNA fragments confer functional changes to high-density lipoproteins in atherosclerosis.

Atherosclerosis·2025
Same author

Oxidized Phospholipids, Lipoprotein(a), and Cardiovascular Outcomes After Acute Coronary Syndrome.

Circulation·2025
Same author

Author Correction: Lack of macrophage fatty-acid-binding protein aP2 protects mice deficient in apolipoprotein E against atherosclerosis.

Nature medicine·2025
Same author

Multiplex Apolipoprotein Panel Improves Cardiovascular Event Prediction and Cardiovascular Outcome by Identifying Patients Who Benefit From Targeted PCSK9 Inhibitor Therapy.

Arteriosclerosis, thrombosis, and vascular biology·2025
Same author

Impact of PREVENT Cardiovascular Risk Equations on Statin Eligibility by Subgroup and Risk Thresholds: A Cross-Sectional Study.

Journal of general internal medicine·2025

Inhibition of cyclooxygenase-2 (COX-2) reduced atherosclerosis in mice. Macrophage COX-2 plays a proatherogenic role, suggesting anti-inflammatory strategies for atherosclerosis prevention.

Area of Science:

  • Cardiovascular Biology
  • Inflammation Research
  • Pharmacology

Background:

  • Cyclooxygenase (COX) enzymes regulate eicosanoids involved in vascular homeostasis and inflammation.
  • COX-1 produces platelet thromboxane A2, while COX-1 and COX-2 produce endothelial prostacyclin.
  • Concerns exist regarding COX-2 inhibitors and thrombotic events due to potential imbalance in thromboxane A2 and prostacyclin.

Purpose of the Study:

  • To investigate the role of cyclooxygenase-2 (COX-2) in atherosclerosis development.
  • To test the hypothesis that pharmacological inhibition of COX-2 reduces early atherosclerosis in LDL-receptor deficient mice.

Main Methods:

  • LDL-receptor deficient mice were fed a Western-type diet and treated with rofecoxib (selective COX-2 inhibitor) or indomethacin (non-selective COX inhibitor).

Related Experiment Videos

  • Macrophage-specific COX-2 deficiency was achieved via fetal liver cell transplantation in LDL-receptor deficient mice.
  • Atherosclerosis progression was assessed and compared between treatment groups and controls.

    • Main Results:

    • Pharmacological inhibition of COX-2 significantly reduced atherosclerosis in LDL-receptor deficient mice.
    • Genetic deletion of macrophage COX-2 also led to significantly less atherosclerosis compared to controls.
    • These findings provide evidence for a proatherogenic role of macrophage COX-2.

    Conclusions:

    • Macrophage cyclooxygenase-2 expression contributes to the development of atherosclerosis.
    • Targeting COX-2 with anti-inflammatory approaches may offer a strategy for atherosclerosis prevention.
    • Further clinical trials are needed to resolve controversies surrounding COX-2 inhibitors and cardiovascular events.