Mitochondrial health, the epigenome and healthspan

Miguel A. Aon, Sonia Cortassa, Magdalena Juhaszova, Steven J. Sollott

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish (US)
Pages (from-to)1285-1305
Number of pages21
JournalClinical Science
Volume130
Issue number15
DOIs
StatePublished - 2016

Keywords

  • Acetylation
  • Aging
  • Autophagy
  • Biogenesis
  • Caloric restriction
  • Cardiovascular disease
  • Chromatin
  • Diet
  • Epigenetic modification
  • Histones
  • Mitochondrial fusion-fission
  • Mitophagy

ASJC Scopus subject areas

  • Medicine(all)

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