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Chemokines in Myocardial Infarction
Bijun Chen1, Nikolaos G Frangogiannis2
1The Wilf Family Cardiovascular Research Institute, Department of Medicine (Cardiology), Albert Einstein College of Medicine, 1300 Morris Park Avenue Forchheimer G46B, Bronx, NY, USA.
Insights
Chemokines orchestrate cardiac repair and adverse remodeling after myocardial infarction. Targeting these inflammatory mediators offers therapeutic potential but faces challenges due to their dual roles in injury and healing.
Area of Science:
- Cardiovascular Biology
- Immunology
- Molecular Medicine
Background:
- Myocardial infarction (MI) induces inflammation, crucial for repair but also linked to heart failure.
- Chemokines (CC and CXC) are upregulated in infarcted hearts, guiding immune cell movement.
- Specific chemokines influence neutrophil and mononuclear cell recruitment, and leukocyte-independent functions.
Purpose of the Study:
- To review the role of chemokines in myocardial infarction.
- To discuss their regulation of cardiac injury, repair, and remodeling.
- To explore therapeutic implications and challenges.
Main Methods:
- Literature review of chemokine function in myocardial infarction.
- Analysis of chemokine roles in leukocyte trafficking and direct cellular modulation.
- Discussion of clinical translation barriers.
Main Results:
- Chemokines are key regulators of inflammatory responses post-MI.
- ELR+ CXC chemokines (e.g., CXCL8) drive neutrophil infiltration.
- CC chemokines (e.g., CCL2) recruit mononuclear cells; some chemokines have leukocyte-independent effects.
Conclusions:
- Chemokines are critical in MI-induced injury, repair, and adverse remodeling.
- While promising therapeutic targets, their broad functions complicate clinical application.
- Further research is needed to harness chemokine pathways for heart failure treatment.
Abstract:
In the infarcted myocardium, cardiomyocyte necrosis triggers an intense inflammatory reaction that not only is critical for cardiac repair, but also contributes to adverse remodeling and to the pathogenesis of heart failure. Both CC and CXC chemokines are markedly induced in the infarcted heart, bind to endothelial glycosaminoglycans, and regulate leukocyte trafficking and function. ELR+ CXC chemokines (such as CXCL8) control neutrophil infiltration, whereas CC chemokines (such as CCL2) mediate recruitment of mononuclear cells. Moreover, some members of the chemokine family (such as CXCL10 and CXCL12) may mediate leukocyte-independent actions, directly modulating fibroblast and vascular cell function. This review manuscript discusses our understanding of the role of the chemokines in regulation of injury, repair, and remodeling following myocardial infarction. Although several chemokines may be promising therapeutic targets in patients with myocardial infarction, clinical implementation of chemokine-based therapeutics is hampered by the broad effects of the chemokines in both injury and repair.
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