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

Chemokines and atherosclerosis.

Yuri Sheikine1, Göran K Hansson

  • 1Center for Molecular Medicine, Cardiovascular Research Unit, Karolinska Institute, Stockholm, Sweden. yuri.sheikine@cmm.ki.se

Annals of Medicine
|May 4, 2004
PubMed
Summary

Chemokines, crucial for inflammation, drive leukocyte accumulation in atherosclerosis. Targeting these signaling pathways offers a promising strategy for anti-atherogenic therapies.

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

NOD1 ligand FK565 promotes atherogenesis and accumulation of NOD1<sup>+</sup> smooth muscle cells in atherosclerotic lesions.

Atherosclerosis·2026
Same author

PCSK6 ablation in blood circulating cells increases atherosclerotic burden, but improves plaque stability by activating Th17-smooth muscle cell modulatory axis.

Vascular pharmacology·2025
Same author

Fgf23 expression increases atherosclerotic plaque burden in male ApoE deficient mice.

Atherosclerosis·2025
Same author

Repetitive Antigen Responses of LDL-Reactive CD4+ T Cells Induce Tr1 Cell-Mediated Immune Tolerance.

Arteriosclerosis, thrombosis, and vascular biology·2023
Same author

Phase III MANIFEST-2: pelabresib + ruxolitinib vs placebo + ruxolitinib in JAK inhibitor treatment-naive myelofibrosis.

Future oncology (London, England)·2022
Same author

Animal Models of Atherosclerosis-Supportive Notes and Tricks of the Trade.

Circulation research·2022

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Molecular Medicine

Background:

  • Atherosclerosis is an inflammatory disease involving leukocyte accumulation in vessel walls.
  • Chemokines are polypeptides that attract cells to inflammatory sites via G-protein coupled receptors.
  • These molecules play critical roles in various physiological and pathological conditions, including atherosclerosis.

Purpose of the Study:

  • To explore the role of chemokines in the development and progression of atherosclerosis.
  • To identify specific chemokines involved in leukocyte trafficking and retention within atherosclerotic plaques.
  • To assess the potential of chemokines and their receptors as clinical markers and therapeutic targets for atherosclerosis.

Main Methods:

  • Review of in vivo and in vitro investigations on chemokine function in inflammation.
  • Analysis of studies examining the expression and function of specific chemokines (e.g., MCP-1, RANTES, CXCL16) in atherosclerosis.
  • Examination of research on viral chemokine homologues and their potential role in pathogenesis.

Main Results:

  • Chemokines like MCP-1, MCP-4, MIP-1, and RANTES mediate leukocyte recruitment and retention in atherosclerotic plaques.
  • CXCL16 exhibits a dual role as both a chemokine and a scavenger receptor.
  • Viral chemokine homologues may contribute to atherosclerosis pathogenesis.
  • Chemokine expression levels and gene polymorphisms show potential as clinical markers for cardiovascular diseases.

Conclusions:

  • Chemokines are key mediators of leukocyte trafficking in atherosclerosis.
  • Targeting chemokine signaling pathways presents a viable anti-atherogenic therapeutic strategy.
  • Chemokines and their receptors hold promise as biomarkers for cardiovascular disease risk and progression.

Related Experiment Videos