Functional Relevance of Macrophage-mediated Inflammation to Cardiac Regeneration

Figures

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  FIG. 1. Prevalence of myocardial infarction and the incidence rate of heart failure in Korea. AMI: acute myocardial infarction, IHD: ischemic heart disease, HF: heart failure, yr: years, mo: months.

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  FIG. 2. The sources of stem cells.

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  FIG. 3. (A) Representative images of immunocytofluorescence staining showed the cardiogenic MSCs expressed cardiac-specific proteins GATA4 (green) and cTnI (red). Nuclei were stained with DAPI (blue). (B) Treatment of MSCs with differentiation inducer upregulated cardiac marker expressions such as MEF2C, cTnI, and GATA4. MSCs: mesenchymal stem cells, MEF2C: myocyte enhancer factor 2c, cTnI: cardiac troponin I.

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  FIG. 4. Mapping images of left ventricle in a porcine myocardial infarction model. red: infarct zone, yellow: peri-infarct zone, green: viable myocardium. Stem cells are injected into the myocardium endocardially by using MYOSTAR injection catheter.

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  FIG. 5. Phenotype changes of infiltrated macrophages in the infarcted myocardium over time. M1 type represents pro-inflammatory macrophages, while M2 represents anti-inflammatory subtype. MI: myocardial infarction, iNOS: inducible nitric oxide synthase, IL-1β: interleukin-1β, TNF-α: tumor necrosis factor-α, Arg1: arginase 1.

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  FIG. 6. Stem cells and small molecules such as 5-azacytidine and BIO modulate multiple aspects of the cardiac microenvironment to improve cardiac remodeling after injury. Cardiomyocytes are protected from cell death to provide a therapeutic opportunity to replace a portion of the dead cardiomyocytes, whereas proliferation of cardiac myofibroblasts was inhibited. Macrophage phenotype was shifted toward anti-inflammatory in the cardiac microenvironment.