Relationship of tobacco smoking and smoking-related DNA methylation with epigenetic age acceleration

摘要: // Xu Gao 1 , Yan Zhang Lutz Philipp Breitling 1,4 and Hermann Brenner 1,2,3 Division of Clinical Epidemiology Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany 2 Preventive Oncology, (DKFZ) National for Tumor Diseases (NCT), 3 Consortium (DKTK), 4 Pneumology Respiratory Critical Care Medicine, Thoraxklinik, University Correspondence to: Brenner, email: Keywords : tobacco smoking, epigenetic clock, age acceleration, AHRR, whole blood sample, Gerotarget Received April 04, 2016 Accepted May 14, Published June 02, Abstract Recent studies have identified biomarkers chronological based on DNA methylation levels. Since active smoking contributes to a wide spectrum aging-related diseases in adults, this study intended examine whether exposure could accelerate the forms acceleration (AA, residuals estimate regressed age). We obtained profiles samples by Illumina Infinium Human Methylation450 Beadchip array two independent subsamples ESTHER calculated their ages recently proposed algorithms. None self-reported indicators (smoking status, cumulative cessation time) or serum cotinine levels was significantly associated with AA. On contrary, we successfully confirmed that 66 out 150 smoking-related CpG sites were AA, even after correction multiple testing (FDR <0.05). further built index (SI) these loci demonstrated monotonic dose-response relationship In conclusion, methylation-based biological current past exposure, but not information levels, found be related defined Further research should address potential mechanisms underlying observed patterns, such as reflections susceptibility environmental hazards both changes