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Copyright ©2014 Baishideng Publishing Group Inc.
World J Cardiol. Sep 26, 2014; 6(9): 939-958
Published online Sep 26, 2014. doi: 10.4330/wjc.v6.i9.939
Figure 1
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Figure 1 Schematic overview of miRNAs involved in apoptosis in myocardial infarction.
Figure 2
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Figure 2 Schematic overview of miRNAs involved in angiogenesis in myocardial infarction.
Figure 3
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Figure 3 Schematic overview of miRNAs involved in fibrosis after myocardial infarction.
Figure 4
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Figure 4 Venn’s diagram of number of differentially expressed miRNAs in human myocardial infarction compared to mouse and rat model of myocardial infarction. Experimental data were obtained from microarray analysis performed on mouse model of MI[32,33], rat model of MI[43,44] and human MI[54,58]. MI: Myocardial infarction.
Figure 5
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Figure 5 Therapeutic opportunities of miRNAs in myocardial infarction identified by using mouse model of myocardial infarction. BMC: Bone marrow cell; ESC: Embryonic stem cell; LV: Left ventricle; MSC: Mesenchymal stem cell; MI: Myocardial infarction; IGF-1: Insulin-like growth factor 1.
Figure 6
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Figure 6 Therapeutic opportunities of miRNAs in myocardial infarction identified by using rat model of myocardial infarction. BM-MSC: Bone marrow-mesenchymal stem cell; LV: Left ventricle; MI: Myocardial infarction; Cx43: Gap junction alpha-1 protein; HCN4: Potassium/sodium hyperpolarization-activated cyclic nucleotide-gated channel 4.