Analysis of the Correlation Between PPARγ Promoter Methylation and Myocardial Infarction
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Abstract
Objective To analyze the correlation between peroxisome proliferator-activated receptor gamma (PPARγ) promoter methylation and myocardial infarction. Methods The research subjects were divided into myocardial infarction group (110 cases) and control group (102 cases). Methylation-specific real-time fluorescence quantitative polymerase chain technology (qMSP) was used to analyze the methylation level of PPARγ gene promoter in the two groups and analysis its correlation with myocardial infarction. Results There was no significant difference in the general data between the myocardial infarction group and the control group (P>0.05). The blood glucose, total cholesterol (TC), triglyceride (TG) and low density lipoprotein (LDL-c) in the myocardial infarction group were significantly higher than those in the control group (P<0.05). The methylation rate of PPARγ promoter in the myocardial infarction group was significantly higher than that in the control group. Regardless of whether methylation occurs in CpG-1 or CpG-2, the expression level of PPARγ mRNA in the methylated group was significantly lower than that in the unmethylated group. In the myocardial infarction group, the methylation level of PPARγ gene promoter region was positively correlated with TC, TG, LDL-c, lipoprotein(a), and negatively correlated with high density lipoprotein (HDL-c). In the control group, the methylation level of PPARγ gene promoter region was positively correlated with age and was statistically significant (P<0.05). Among diabetic patients in the myocardial infarction group, the methylation level of the PPARγ gene promoter region was positively correlated with the degree of stenosis, and was statistically significant (P<0.05). Conclusions There was correlation between PPARγ promoter methylation and myocardial infarction, and its decrease may play a protective role in myocardial infarction, and it may be a new target for the treatment of myocardial infarction.
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