Long-term PM2.5 exposure is implicated in cardiometabolic disorders, but its interactions with genetic susceptibility and the underlying epigenetic mechanisms remain unclear. We sought to examine the joint associations of long-term PM2.5 exposure and genetic susceptibility with prevalent metabolic syndrome (MetS) and subsequent cardiovascular disease (CVD) risk among individuals with MetS. Among 324,887 UK Biobank participants, logistic regression analyses indicated greater odds of MetS at higher PM2.5 exposure (adjusted OR = 1.04, 95% CI: 1.03-1.05). Among 64,832 individuals with MetS, Cox regression with inverse probability weighting showed elevated incident CVD risk at higher PM2.5 exposure (adjusted HR = 1.04, 95% CI: 1.01-1.06). Additive interaction analyses revealed significant synergy of PM2.5 exposure with both the polygenic risk score (PRS) for MetS (relative excess risk due to interaction [RERI] = 0.11, 95% CI: 0.02-0.20) and the PRS for CVD (RERI = 0.13, 95% CI: 0.05-0.21). 1 PM2.5-associated CpG site related to MetS and five related to CVD were identified by summary-data-based Mendelian randomization (SMR) analyses. Among these, cg13235717 near SFN emerged as a key locus across phenotypes, and gene-environment interaction analyses further supported its potential role as an epigenetic modifier. Overall, these findings indicate that long-term PM2.5 exposure is associated with prevalent MetS and subsequent CVD risk among individuals with MetS, particularly among genetically susceptible individuals, with DNA methylation potentially serving as an epigenetic link in these associations.
Zi-Yue Li, Hao-Zhang Huang, Jin-Ming Chen et al.· Ecotoxicology and Environmen...· 0 citations
BACKGROUND
Patients with atherosclerotic cardiovascular disease (ASCVD) have a high risk of recurrent major adverse cardiovascular events (MACE) and chronic kidney disease (CKD). Although Life's Essential 8 (LE8) has been studied for cardiovascular outcomes in secondary prevention, systematic evaluations of its association with cardiorenal events remain lacking.
OBJECTIVES
To evaluate whether optimal cardiovascular health (CVH) was associated with lower risks of MACE and CKD in ASCVD patients.
METHODS
This study included 10,253 UK Biobank participants with ASCVD, categorized into low (<50), moderate (50‒79), and high (≥80) CVH groups by LE8 score. Associations with MACE and CKD were assessed using Fine-Gray regression models, population-attributable fractions (PAF), and 1:2 propensity-matched analyses versus 16,545 non-ASCVD participants.
RESULTS
During a median 13.3 years follow-up, 2,069 MACE and 1,290 CKD events occurred. Compared with high CVH, low CVH was associated with higher risks of MACE (subdistribution HR [sHR] 2.68, 95% CI 2.02-3.56, p <0.001) and CKD (sHR 2.34, 95% CI 1.57-3.48, p <0.001). Glucose control contributed the largest PAF to both MACE (10.5%) and CKD (15.1%), followed by smoking cessation (6.9% for MACE and 11.1% for CKD). Compared with matched non-ASCVD participants, ASCVD patients with high LE8 attenuated MACE (sHR 0.83, 95% CI 0.58-1.20; p = 0.33) and CKD (sHR 0.69, 95% CI 0.42-1.13; p = 0.14) risks.
CONCLUSIONS
Higher LE8 scores were associated with lower risks of MACE and CKD in ASCVD patients. Glucose control and smoking were key modifiable contributors. High LE8 achievement may attenuate risks toward non-ASCVD levels.
This study reveals that SRA1 is a novel therapeutic target for PPD, which enhances the understanding of its molecular aetiology and the development of therapeutic strategies.
Ming Chen, Qinlin Wei, Hao-Wen Li et al.· npj Mental Health Research· 0 citations
Findings highlight significant sex differences in the effect of depression on CHD risk, which could inform sex-specific preventive strategies for reducing the cardiovascular burden in individuals with depression.
Haozhang Huang, Ming Chen, Xiao-Zhao Lu et al.· European Journal of Preventi...· 0 citations
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