We hypothesized that CHIP overall and gene-specific CHIP mutations would be associated with distinct DNAm signatures, given the roles of DNMT3A and TET2 in regulating DNAm. In this study, we conducted multi-ancestry epigenome-wide association meta-analysis of CHIP, followed by enrichment analysis and functional annotation of associated CpG loci, and mediation analysis and Mendelian randomization to examine the potential interplay between CHIP and DNAm in aging and disease.
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