Korean Circ J.  2009 Oct;39(10):393-398. 10.4070/kcj.2009.39.10.393.

The Inflammatory Response and Cardiac Repair After Myocardial Infarction

• Nah DY
• Rhee MY

• KMID: 2028918
• DOI: http://doi.org/10.4070/kcj.2009.39.10.393

Abstract

One of the most important therapeutic targets of current cardiology practice is to determine optimal strategies for the minimization of myocardial necrosis and optimization of cardiac repair following an acute myocardial infarction. Myocardial necrosis after acute myocardial infarction induces complement activation and free radical generation, triggering a cytokine cascade initiated by tumor necrosis factor-alpha (TNF-alpha) release. When reperfusion of the infarcted area is initiated, intense inflammation follows. Chemokines, cytokines and the complement system play an important role in recruiting neutrophils in the ischemic and reperfused myocardium. Cytokines promote adhesive interactions between leukocytes and endothelial cells, resulting in transmigration of inflammatory cells into the site of injury. The recruited neutrophils have potent cytotoxic effects through the release of proteolytic enzymes, and they interact with adhesion molecules on cardiomyocytes. In spite of the potential injury, reperfusion enhances cardiac repair; this may be related to the inflammatory response. Monocyte chemoattractant protein (MCP)-1 is upregulated in reperfused myocardium and can induce monocyte recruitment in the infarcted area. Monocyte subsets play a role in phagocytosis of dead cardiomyocytes and in granulation tissue formation. In addition, the transforming growth factor (TGF)-beta plays a crucial role in cardiac repair by suppressing inflammation. Resolution of inflammatory infiltration, containment of inflammation and the reparative response affecting the infarcted area are essential for optimal infarct healing. Here, we review the current literature on the inflammatory response and cardiac repair after myocardial infarction.

Keyword

Myocardial infarction; Inflammation; Left ventricle remodeling; Cytokines

MeSH Terms

Adhesives
Cardiology
Chemokines
Complement Activation
Complement System Proteins
Containment of Biohazards
Cytokines
Endothelial Cells
Granulation Tissue
Inflammation
Leukocytes
Monocytes
Myocardial Infarction
Myocardium
Myocytes, Cardiac
Necrosis
Neutrophils
Peptide Hydrolases
Phagocytosis
Reperfusion
Reperfusion Injury
Transforming Growth Factors
Tumor Necrosis Factor-alpha
Ventricular Remodeling
Adhesives
Chemokines
Complement System Proteins
Cytokines
Peptide Hydrolases
Transforming Growth Factors
Tumor Necrosis Factor-alpha

Figure

• 

  Fig. 1 The phases of healing in murine myocardial infarction.

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