Purpose of review: The quest for factors and mechanisms responsible for aberrant DNA methylation in human disease-including atherosclerosis-is a promising area of research. This review focuses on the role of fatty acids (FAs) as modulators of DNA methylation-in particular the role of mitochondrial beta-oxidation in FA-induced changes in DNA methylation during the progression of atherosclerosis.
Recent findings: Recent publications have advanced the knowledge in all areas touched by this review: the causal role of lipids in shaping the DNA methylome, the associations between chronic degenerative disease and mitochondrial function, the lipid composition of the atheroma, and the relevance of DNA hypermethylation in atherosclerosis. Evidence is beginning to emerge, linking the dynamics of FA type abundance, mitochondrial function, and DNA methylation in the atheroma and systemically. In particular, this review highlights mitochondrial beta-oxidation as an important regulator of DNA methylation in metabolic disease. Despite the many questions still unanswered, this area of research promises to identify mechanisms and molecular factors that establish a pathological gene expression pattern in atherosclerosis.
Keywords: Atherosclerosis; Beta-oxidation; DNA methylation; Fatty acids; Mitochondrial dysfunction; Noncommunicable disease.