Background Myocardial infarction (MI) remains the leading cause of death and disability among cardiovascular diseases worldwide. Studies show that elevated low-density lipid protein cholesterol (LDL-C) levels confer the highest absolute risk of MI, and Apolipoprotein E (ApoE) is implicated in regulating levels of triglycerides (TGs), cholesterol, and LDL-C. Our study aimed to evaluate the association between APOE polymorphism and MI, and to provide evidence for the etiology of MI. Methods Case–control studies on the association between APOE polymorphisms and the risk of myocardial infarction were included by searching PubMed, Web of Science, and CNKI, and this meta-analysis was written in accordance with PRISMA guideline statement. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using either random-effects or fixed-effects models by R software. Results A total of 33 eligible articles involving 13,706 cases and 14,817 controls were finally selected. The pooled analysis based on the total eligible articles showed that the risk of MI was associated with ApoE epsilon 2 and epsilon 4 alleles. The results showed that patients with MI had a low frequency of the ε2 allele (OR 0.74, 95% CI 0.64–0.86) and a high frequency of the ε4 allele (OR 1.24, 95% CI 1.09–1.42). Conclusions APOE ε2-involved genotypes may be protective factors for MI; in contrast, ε4-involved genotypes (ε4/ε3 vs. ε3/ε3, and ε4/ε4 vs. ε3/ε3) may be risk factors for MI.

Background Multimorbidity is defined as two or more chronic health conditions existing in an individual simultaneously. Multimorbidity has been associated with poor conditions, such as higher health care costs and the poor quality of life. Thus, identifying the risk factors of the multimorbidity is required for multimorbidity prevention. Methods This study was based on the Comprehensive Demonstration Research Project of Major Chronic Noncommunicable Disease Prevention and Control Technology in Northeast China initiated by China Medical University. The investigation was a cross-sectional study under a multistage stratified cluster random sampling design. Associations between multimorbidity and sociodemographic and behavioral factors in adult residents were investigated using univariate analysis and multivariate logistic regression analysis. Results A total of 6706 participants were enrolled in this investigation, and the prevalence of multimorbidity was 21.2% among the adult residents of northeastern China. There existed differences of association between age and multimorbidity risks (65–69 years old: OR = 3.53, 95%CI: 2.04–6.12; 70–74 years old: OR = 5.26, 95%CI: 3.02–9.17). Participants who are overweight had significantly high multimorbidity risk (OR = 2.76, 95%CI: 1.50–5.24). Family history of hypertension and family history of diabetes were significantly associated with high multimorbidity risk (family history of hypertension: OR = 2.34, 95%CI: 1.96–2.79; family history of diabetes: OR = 1.77, 95%CI: 1.38–2.26). Compared with the frequency of fatigue (< 1 time/week or 1–2 times/week), that (≥3 times/week) was associated with high multimorbidity risk (OR = 1.39, 95%CI: 1.07–1.81). For fresh fruit consumption, compared with eating fruits regularly, eating rarely had a higher risk of multimorbidity (OR = 2.33, 95%CI: 1.90–2.85). Conclusions Sociodemographic indices (age, BMI, family history of hypertension, and family history of diabetes) and behavioral indices (fatigue status and fresh fruit consumption) increase the risks of multimorbidity. This study provides a necessary route to prevent and control multimorbidity in northeast China.

Background: Dysfunction of endothelial cells links to microvascular rarefaction, reflecting the pathogenesis of hypertension. Our previous studies found that miR-3656 reduces nitric oxide generation and von Willebrand factor (vWF) cleavage, thereby retarding blood flow and potentially increasing blood pressure. In this paper, we investigated mechanism of transcription regulation contributing to miR-3656-damaged endothelial cells in hypertension. Methods:The effects of miR-3656 on function of endothelial cells were analyzed on the basis of proliferation, migration, tube formation, and apoptosis. The mRNA level and protein level of genes were examined using quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Dual-luciferase reporter assay was performed to confirm the binding between miR-3656 and 3' untranslated region (UTR) of transcription factor AP-2 gamma (TFAP2C). The binding between TFAP2C and the promoter region of Krppel-like factor 10 (KLF10) was confirmed by chromatin immunoprecipitation-qPCR assay.Results: miR-3656 impaired the cell proliferation, migration, tube formation, and apoptosis of endothelial cells. miR-3656 inhibited the expression of TFAP2C by directly targeting 3'UTR of TFAP2C; moreover, miR-3656induced injury of endothelial cells was rescued by TFAP2C overexpression. Furthermore, downregulated TFAP2C decreased KLF10 expression by binding to KLF10 promoter region, and upregulated KLF10 reversed the effects of silencing TFAP2C on endothelial cells. These inhibitory processes led to interference of miR-3656 to KLF10promoted function of endothelial cells. Conclusion:TFAP2C/KLF10 axis is involved in miR-3656related dysfunction of endothelial cells in hypertension. The 3'UTR of TFAP2C and KLF10 promoter region are the hubs of the TFAP2C/KLF10 axis.

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