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Laminar Flow-based Assays to Investigate Leukocyte Recruitment on Cultured Vascular Cells and Adherent Platelets
Published on: April 9, 2018
Leukocyte recruitment in atherosclerosis: potential targets for therapeutic approaches?
1Cardiology Division, Department of Medicine, Geneva University Hospital, Foundation for Medical Research, 64 Avenue Roseraie, 1211 Geneva, Switzerland.
Insights
Atherosclerosis involves complex inflammatory processes and cellular interactions. Understanding leukocyte migration and intercellular communication offers new therapeutic targets for cardiovascular disease.
Area of Science:
- Cardiovascular biology
- Immunology
- Pathophysiology
Background:
- Atherosclerosis is a complex inflammatory disease driven by cellular interactions.
- Vascular injury and endothelial dysfunction promote inflammatory marker expression and leukocyte migration.
- Leukocyte recruitment into the vessel intima is critical for disease development.
Purpose of the Study:
- To review recent findings on leukocyte migration in atherosclerosis.
- To discuss the roles of chemokines, receptors, adhesion molecules, and gap junctions.
- To explore potential therapeutic strategies targeting these cellular processes.
Main Methods:
- Review of current scientific literature on leukocyte migration in atherosclerosis.
- Synthesis of data on molecular mechanisms involved in leukocyte recruitment.
- Discussion of emerging therapeutic targets.
Main Results:
- Chemokines, receptors, adhesion molecules, and gap junctions are key regulators of leukocyte migration.
- These molecules facilitate leukocyte arrest, transmigration, and intercellular communication.
- Targeting these pathways presents potential therapeutic avenues.
Conclusions:
- Leukocyte migration is a central process in atherosclerosis pathogenesis.
- Intercellular communication molecules play significant roles in leukocyte recruitment.
- Targeting leukocyte migration and communication pathways may offer novel treatments for atherosclerosis.
Abstract:
Atherosclerosis is a complex inflammatory disease involving cellular migration and interaction. Vascular injury in response to different cardiovascular risk factors enhances endothelial dysfunction, which in turn promotes the expression of inflammatory markers and transendothelial leukocyte migration. Recruitment of leukocytes from the blood stream into the vessel intima is a crucial step for the development of the disease. Recent findings have highlighted the role of chemokines, chemokine receptors, adhesion molecules, and gap junctions in this process by acting as chemoattractant, adhesive, or intercellular communication molecules. In this short review, we summarize new data concerning the different steps from leukocyte arrest to transendothelial migration and discuss potential new therapeutic approaches concerning these processes.
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