title: Mitochondrial health, the epigenome and healthspan.
abstract: Food nutrients and metabolic supply-demand dynamics constitute environmental factors that interact with our genome influencing health and disease states. These gene-environment interactions converge at the metabolic-epigenome-genome axis to regulate gene expression and phenotypic outcomes. Mounting evidence indicates that nutrients and lifestyle strongly influence genome-metabolic functional interactions determining disease via altered epigenetic regulation. The mitochondrial network is a central player of the metabolic-epigenome-genome axis, regulating the level of key metabolites [NAD(+), AcCoA (acetyl CoA), ATP] acting as substrates/cofactors for acetyl transferases, kinases (e.g. protein kinase A) and deacetylases (e.g. sirtuins, SIRTs). The chromatin, an assembly of DNA and nucleoproteins, regulates the transcriptional process, acting at the epigenomic interface between metabolism and the genome. Within this framework, we review existing evidence showing that preservation of mitochondrial network function is directly involved in decreasing the rate of damage accumulation thus slowing aging and improving healthspan.
authors.affiliation: Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, U.S.A. miguel.aon@nih.gov.
authors.forename: Miguel A
authors.initials: MA
authors.lastname: Aon
authors.affiliation: Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, U.S.A.
authors.forename: Sonia
authors.initials: S
authors.lastname: Cortassa
authors.affiliation: Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, U.S.A.
authors.forename: Magdalena
authors.initials: M
authors.lastname: Juhaszova
authors.affiliation: Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, U.S.A.
authors.forename: Steven J
authors.initials: SJ
authors.lastname: Sollott
mesh_terms: D000293:Adolescent; D000328:Adult; D000367:Age Factors; D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D002648:Child; D002675:Child, Preschool; D004272:DNA, Mitochondrial / Q000235:genetics / Q000378:metabolism; D004734:Energy Metabolism; D044127:Epigenesis, Genetic; D005786:Gene Expression Regulation; D059647:Gene-Environment Interaction; D015894:Genome, Human; D006304:Health Status; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008019:Life Style; D008136:Longevity; D008875:Middle Aged; D008928:Mitochondria / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D009154:Mutation; D009752:Nutritional Status; D055815:Young Adult
chemical_list: D004272:DNA, Mitochondrial
keywords: acetylation; adipose tissue; aging; autophagy; biogenesis; caloric restriction; cardiovascular disease; chromatin; diet; epigenetic modification; epigenetics; histones; mitochondria; mitochondrial fusion–fission; mitophagy