Correlation between Furin promoter methylation levels and blood pressure of non-diabetic population in a community
- VernacularTitle:Furin启动子甲基化水平与社区非糖尿病人群血压的相关性
- Author:
Wei JIA
1
;
Zhi TIAN
Author Information
- Publication Type:Journal Article
- Keywords: hypertension; Furin; promoter regions,genetic; methylation; non-diabetes
- From: Tianjin Medical Journal 2025;53(9):987-992
- CountryChina
- Language:Chinese
- Abstract: Objective To investigate the correlation between Furin promoter methylation level and blood pressure in a community-based non-diabetic population.Methods A secondary analysis was conducted on the research data from a study in the Dryad open database regarding the methylation rate of Furin promoter and the risk of diabetes.After including the participants from the original data and excluding those with a history of cardiovascular disease,diabetes or diagnosed diabetes at the time of enrollment,those lacking blood samples,those who refused to participate in follow-up examinations,those who died during the follow-up period and those with missing data,a total of 1 832 subjects formed the community non-diabetic population.The methylation rates of 8 CpG sites in the Furin promoter region,fasting blood glucose,lipid and blood pressure were collected at baseline.The subjects were divided into the normal systolic blood pressure(SBP)group(1 388 cases)and the elevated SBP group(444 cases)based on whether SBP was≥140 mmHg,the diastolic blood pressure(DBP)was≥90 mmHg and the hypertension diagnostic criteria(SBP≥140 mmHg or DBP≥90 mmHg.There were 1 341 cases in the normal DBP group,491 cases in the elevated DBP group and 1 218 cases in the normal blood pressure group.A multivariate linear regression model was used to observe the correlation between the methylation rate of the Furin promoter and changes of SBP and DBP.For the Furin promoter methylation sites independently related to SBP/DBP.Linear regression models adjusted for confounding factors were used to fit the curve to observe whether there was a non-linear relationship between SBP or DBP and the methylation rate of the Furin promoter,respectively.Unadjusted and adjusted Logistic regression models were used to observe the correlation between the methylation rate of the Furin promoter and the risk of hypertension.The adjustment factors in the adjusted Logistic regression model were identical to those in the linear regression fitting curve.Results Compared with the normal SBP group,the methylation rates of CpG1,CpG2 and CpG4 were decreased in the elevated SBP group,while the methylation rate of CpG8 was increased(P＜0.05).Compared with the normal DBP group,the methylation rates of CpG2 and CpG4 were decreased in the elevated DBP group,while the methylation rate of CpG8 was increased(P＜0.01).Compared with the normal blood pressure group,the methylation rates of CpG1,CpG2,CpG4 and CpG6 were decreased in the hypertension group,while the methylation rate of CpG8 was increased(P＜0.05).Multivariate linear regression analysis showed that the decreased methylation rate at the CpG2 site and the increased methylation rate at the CpG8 site were independently associated with elevated SBP and DBP.The linear regression model fitting curves indicated that the increased methylation rate at the CpG2 site was linearly related to the decrease in SBP/DBP(P values for non-linearity were 0.143 and 0.481,respectively),and the increased methylation rate at the CpG8 site was linearly related to the increase in SBP/DBP(P values for non-linearity were 0.727 and 0.940,respectively).Unadjusted Logistic regression analysis showed that the methylation rates of CpG2 and CpG8 were influencing factors of hypertension(P＜0.01).Adjusted Logistic regression analysis showed that the increased methylation rate at the CpG2 site was independent protective factors,and the increased methylation rate at the CpG8 site was independent risk factor for hypertension(P＜0.01).Conclusion The methylation levels at the CpG2 and CpG8 sites of the Furin promoter are independent factors associated with blood pressure changes in the non-diabetic population in the community.
