Mitochondrial health, the epigenome and healthspan.
Mitochondrial health, the epigenome and healthspan.
复制标题
DOI：
10.1042/cs20160002
复制
发表时间：
2016-08-01
期刊：
影响因子：
--
通讯作者：
Sollott SJ
中科院分区：
文献类型：
--
作者：
Aon MA;Cortassa S;Juhaszova M;Sollott SJ
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, ATP) acting as substrates/cofactors for acetyl transferases, kinases (e.g., protein kinase A), deacetylases (e.g., sirtuins). 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.
