ABSTRACT
A large body of evidence spanning at least six decades has demonstrated that atherosclerosis is associated with mitochondrial dysfunction. Reactive oxygen species, lipids, and other cellular components have been intensively studied to understand the impact of mitochondrial function on atherogenesis. Here, we present the evidence supporting the concept and underline the gaps in knowledge and inconsistencies in the field. In particular, we gather the current knowledge on the growing field of mitochondria-to-nucleus retrograde signalling, i.e., the study of factors produced by the mitochondria, that potentially impose an atherogenic epigenome. Furthermore, we discuss results of epigenomics approaches that corroborate the fundamental role of mitochondria in determining risk and progression of atherosclerosis.
