
Clinical Epigenetics, Год журнала: 2025, Номер 17(1)
Опубликована: Янв. 2, 2025
To explore the mechanisms linking smoking to cardiovascular diseases (CVDs) from an epigenetic perspective. Mendelian Randomization (MR) analysis was performed assess causal effects of behavior and DNA methylation levels at smoking-related CpG sites on nine CVDs, including aortic aneurysm, atrial fibrillation, coronary atherosclerosis, heart disease, failure, intracerebral hemorrhage, ischemic stroke, myocardial infarction, subarachnoid hemorrhage. Colocalization used further identify key MR estimates. Reactome enrichment elucidate potential mechanisms. indicates that behaviors are significantly associated with increased risk CVDs (OR > 1, P < 0.05). Through colocalization analysis, five were ultimately determined. alteration cg25313468 (located in TSS1500 region REST) is simultaneously infarction. Additionally, cg21647257 TSS200 CLIP3) fibrillation; cg06197751 SGEF gene body) cg07520810 ARID5B atherosclerosis; cg16822035 MCF2L Enrichment suggests phosphatase tensin homologue (PTEN) may be involved downstream (REST). This study uncovers relationship between smoking, methylation, providing new insights into pathogenic effect
Язык: Английский