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- W2466333622 endingPage "1305" @default.
- W2466333622 startingPage "1285" @default.
- W2466333622 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." @default.
- W2466333622 created "2016-07-22" @default.
- W2466333622 creator A5020291322 @default.
- W2466333622 creator A5036417376 @default.
- W2466333622 creator A5055309835 @default.
- W2466333622 creator A5081151780 @default.
- W2466333622 date "2016-06-29" @default.
- W2466333622 modified "2023-10-12" @default.
- W2466333622 title "Mitochondrial health, the epigenome and healthspan" @default.
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