Related Experiment Video

Updated: Aug 21, 2026

A Novel Three-dimensional Flow Chamber Device to Study Chemokine-directed Extravasation of Cells Circulating under Physiological Flow Conditions
10:56

A Novel Three-dimensional Flow Chamber Device to Study Chemokine-directed Extravasation of Cells Circulating under Physiological Flow Conditions

Published on: July 15, 2013

Chemokines in the pathogenesis of vascular disease

Israel F Charo1, Mark B Taubman

  • 1Gladstone Institute of Cardiovascular Disease, PO Box 419100, San Francisco, CA 94141-9100, USA. icharo@gladstone.ucsf.edu

Circulation Research
|October 30, 2004
PubMed

Insights

Chemokines, like monocyte chemoattractant protein 1 (MCP-1), are key in recruiting leukocytes to inflamed vessels, driving vascular disease. Targeting MCP-1 and its receptor CCR2 offers a promising therapeutic strategy for atherosclerosis and thrombosis.

Area of Science:

  • Immunology
  • Cardiovascular Biology
  • Molecular Medicine

Background:

  • Inflammation is increasingly recognized as a critical factor in vascular diseases.
  • Leukocyte migration from blood to vessel walls is a key inflammatory process.
  • Chemokines are small secreted proteins that orchestrate leukocyte recruitment.

Purpose of the Study:

  • To review the roles of chemokines in leukocyte migration to sites of vascular injury, inflammation, and atherosclerosis.
  • To highlight the specific involvement of monocyte chemoattractant protein 1 (MCP-1) and its receptor CCR2.
  • To discuss the therapeutic potential of targeting chemokine pathways in vascular diseases.

Main Methods:

  • Review of existing literature on chemokines and leukocyte trafficking in vascular disease.
  • Summary of the mechanisms by which chemokines induce chemotaxis via G-protein-coupled receptors.
  • Analysis of the role of MCP-1/CCR2 in monocyte recruitment, intimal hyperplasia, and thrombosis.

Main Results:

  • Chemokines selectively recruit monocytes, neutrophils, and lymphocytes to inflamed vascular sites.
  • Monocyte chemoattractant protein 1 (MCP-1), via CCR2, is crucial for early monocyte recruitment in atherosclerosis and intimal hyperplasia.
  • MCP-1 may contribute to thrombus formation by promoting tissue factor generation, impacting acute thrombosis.

Conclusions:

  • Chemokines, particularly MCP-1/CCR2, play pivotal roles in the pathogenesis of vascular diseases like atherosclerosis and thrombosis.
  • MCP-1/CCR2 are significant therapeutic targets for managing vascular inflammation and its complications.
  • Development of specific antagonists for MCP-1 and related chemokines is a key focus for future therapies.

More Related Videos

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation12:55

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation

Published on: December 9, 2021

Related Concept Videos

Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
Mechanism of Angiogenesis01:10

Mechanism of Angiogenesis

Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...
Inflammation01:38

Inflammation

Overview
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

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...
Acute Inflammation II: Cellular Phase01:26

Acute Inflammation II: Cellular Phase

The cellular phase of acute inflammation is a tightly orchestrated sequence of events that recruits leukocytes, primarily neutrophils, to sites of tissue injury or infection. Following the initial vascular changes, this phase ensures effective immune cell migration, activation, and function at the affected site to eliminate pathogens and initiate tissue repair.Leukocyte Recruitment CascadeLeukocyte recruitment happens in four steps: margination, adhesion, transmigration, and chemotaxis. Reduced...