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Updated: Jun 27, 2025
Flow Cytometry Analysis of Immune Cells Within Murine Aortas
Published on: July 1, 2011
Targeting immune cell recruitment in atherosclerosis
Yvonne Döring1,2,3,4, Emiel P C van der Vorst5,6,7,8, Christian Weber9,10,11,12
1Department of Angiology, Swiss Cardiovascular Center, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. yvonne.doering@unibe.ch.
Insights
Atherosclerosis involves chronic inflammation driven by leukocyte infiltration. New research explores targeted therapies to block this process, offering hope for treating cardiovascular diseases like heart attack and stroke.
Area of Science:
- Cardiovascular Research
- Immunology
- Inflammation Biology
Background:
- Atherosclerosis, a leading cause of myocardial infarction and stroke, involves chronic inflammation in arteries.
- Leukocyte infiltration into the arterial wall, triggered by hyperlipidemia, drives atherosclerotic plaque development.
- Current therapeutic strategies targeting leukocytes in atherosclerosis face challenges in clinical translation due to lack of specificity.
Purpose of the Study:
- To review recent research on receptor-ligand interactions regulating leukocyte influx in atherosclerosis.
- To explore pharmacological interventions targeting these interactions.
- To discuss mechanisms of inflammation resolution and their therapeutic potential.
Main Methods:
- Review of current literature on leukocyte trafficking in atherosclerosis.
- Analysis of pharmacological interventions targeting specific molecular pathways.
- Examination of studies investigating inflammation resolution mechanisms.
Main Results:
- Identified key receptor-ligand pairs and interactors governing leukocyte recruitment in atherosclerotic arteries.
- Highlighted the limitations of current broad-spectrum anti-leukocyte therapies.
- Discussed the potential of targeting specific molecular interactions for improved therapeutic outcomes.
Conclusions:
- Targeting specific leukocyte-endothelial interactions offers a promising strategy for atherosclerotic cardiovascular disease therapy.
- Developing tissue-specific and selective inhibition strategies is crucial for clinical translation.
- Understanding inflammation resolution pathways may reveal novel therapeutic avenues.
Abstract:
Atherosclerosis is the primary underlying cause of myocardial infarction and stroke. Atherosclerotic cardiovascular disease is characterized by a chronic inflammatory reaction in medium-to-large-sized arteries, with its onset and perpetuation driven by leukocytes infiltrating the subendothelial space. Activation of endothelial cells triggered by hyperlipidaemia and lipoprotein retention in the arterial intima initiates the accumulation of pro-inflammatory leukocytes in the arterial wall, fostering the progression of atherosclerosis. This inflammatory response is coordinated by an array of soluble mediators, namely cytokines and chemokines, that amplify inflammation both locally and systemically and are complemented by tissue-specific molecules that regulate the homing, adhesion and transmigration of leukocytes. Despite abundant evidence from mouse models, only a few therapies targeting leukocytes in atherosclerosis have been assessed in humans. The major challenges for the clinical translation of these therapies include the lack of tissue specificity and insufficient selectivity of inhibition strategies. In this Review, we discuss the latest research on receptor-ligand pairs and interactors that regulate leukocyte influx into the inflamed artery wall, primarily focusing on studies that used pharmacological interventions. We also discuss mechanisms that promote the resolution of inflammation and highlight how major findings from these research areas hold promise as potential therapeutic strategies for atherosclerotic cardiovascular disease.
