Figure 1. Schematic representation of hypothesized mechanisms linking DNA methylation to aortic aneurysm progression. This figure highlights: 1) the potential impact of gene body hypermethylation on gene expression, and the complex relationship between promoter and gene body methylation in regulating FBN1 with HI mutational type; 2) the potential of DNMT and TET enzymes, and other methylation-modifying substances, as research tools and therapeutic agents; and 3) the involvement of lysyl oxidases, MMPs, IL-17RA, and genes within the TGF-β and PI3K/AKT pathways, including other potentially methylation-regulated genes. Me: methylation; HI: haploinsufficiency; TGF-β: transforming growth factor-beta; MMPs: matrix metalloproteases; DNMT: DNA methyltransferases; TET: ten-eleven translocation.