Conclusions: We found significant promoter hypomethylation of genes typical for proinflammatory M1-M phi s and hypermethylation of anti-inflammatory, proangiogenic M2-M phi genes in hyperlipidemia and T2DM ischemic muscles. Epigenetic alterations modify M phi phenotype toward proinflammatory M1 as opposed to anti-inflammatory, proangiogenic, and tissue repair M2 phenotype, which may contribute to the impaired adaptive vascular growth under these pathological conditions.