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

CD40 signaling and plaque instability.

U Schönbeck1, P Libby

  • 1Leducq Center for Cardiovascular Research, Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.

Circulation Research
|December 12, 2001
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

Randomised clinical trial: gastrointestinal events in arthritis patients treated with celecoxib, ibuprofen or naproxen in the PRECISION trial.

Alimentary pharmacology & therapeutics·2018
Same author

Inflammation and plaque vulnerability.

Journal of internal medicine·2015
Same author

Neutrophil extracellular traps form predominantly during the organizing stage of human venous thromboembolism development.

Journal of thrombosis and haemostasis : JTH·2014
Same author

Cardiac transplant graft arteriosclerosis.

Trends in cardiovascular medicine·2011
Same author

Molecular imaging of macrophage protease activity in cardiovascular inflammation in vivo.

Thrombosis and haemostasis·2011
Same author

How our growing understanding of inflammation has reshaped the way we think of disease and drug development.

Clinical pharmacology and therapeutics·2010
Same journal

Mitochondrial STING Governs Glycolytic Reprogramming in Diabetic Cardiomyopathy.

Circulation research·2026
Same journal

Hypoxia-Induced Epas1-Myl9/12 Axis Shapes the Pathology of Pulmonary Hypertension.

Circulation research·2026
Same journal

Proteogenomics of Hypertrophic Cardiomyopathy Reveals Subtype-Specific Therapy.

Circulation research·2026
Same journal

Impaired Endothelial Cell Cholesterol Metabolism Promotes Vascular Inflammation in Sleep Apnea.

Circulation research·2026
Same journal

Engineered Heart Tissues Facilitate Noncoding Variant Studies in Cardiomyopathy.

Circulation research·2026
Same journal

NUAK1 Inhibition Alleviates Ischemia-Reperfusion Injury via SYNE1-YAP1.

Circulation research·2026
See all related articles

Blocking CD40/CD40L interactions reduces atherosclerosis development and promotes plaque stabilization. This immune pathway is a promising therapeutic target for cardiovascular disease.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Inflammation Research

Background:

  • Atherosclerosis is increasingly recognized as a chronic inflammatory condition.
  • The immune system plays a critical role in the development of atherosclerotic plaques.
  • Overexpression of CD40 and CD40 ligand (CD40L) is observed in atherosclerotic lesions.

Purpose of the Study:

  • To investigate the role of CD40/CD40L interactions in atherogenesis.
  • To evaluate the therapeutic potential of targeting CD40/CD40L signaling in atherosclerosis.

Main Methods:

  • In vivo studies involving interruption of CD40/CD40L signaling in mouse models of atherosclerosis.
  • In vitro studies examining CD40 ligation on endothelial cells, smooth muscle cells, and macrophages.

Related Experiment Videos

Main Results:

  • Interruption of CD40/CD40L interactions reduced the formation and progression of atherosclerotic plaques in mice.
  • CD40 signaling blockade led to plaque stabilization, characterized by changes in lesion biology and structure.
  • In vitro, CD40 ligation on key cell types promoted pro-atherogenic functions, including the expression of inflammatory mediators and matrix-degrading enzymes.

Conclusions:

  • CD40/CD40L interactions play a central role in promoting atherosclerosis.
  • Targeting the CD40/CD40L pathway represents a novel therapeutic strategy for atherosclerosis.