Mitochondrial epigenetics in aging and cardiovascular diseases

Mitochondria are cellular organelles which generate adenosine triphosphate (ATP) molecules for the maintenance of energy through oxidative phosphorylation. They also regulate a variety processes including apoptosis and metabolism. Of interest, inner part mitochondria—the mitochondrial matrix—contains circular molecule DNA (mtDNA) characterised by its own transcriptional machinery. As with genomic DNA, mtDNA may undergo nucleotide mutations that have been shown to be responsible dysfunction. During physiological aging, membrane potential declines associates enhanced mitophagy avoid accumulation damaged organelles. Moreover, if dysfunctional mitochondria not properly cleared, this could lead dysfunction subsequent development several comorbidities such as cardiovascular diseases (CVDs), diabetes, respiratory well inflammatory disorders psychiatric diseases. reported is amenable chemical modifications, namely methylation. Changes in methylation associated altered programs during aging. In addition, other epigenetic signals observed mitochondria, particular interaction between non-coding RNAs. Mitoepigenetic modifications involved pathogenesis CVDs where oxygen chain disruption, fission, ROS formation alter cardiac metabolism leading hypertrophy, hypertension, heart failure ischemia/reperfusion injury. present review, we summarize current evidence on growing importance changes modulator function A better understanding landscape pave way personalized therapies prevent age-related