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. 2022 Apr 7;119(2):357–370. doi: 10.1093/cvr/cvac058

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© The Author(s) 2022. Published by Oxford University Press on behalf of the European Society of Cardiology.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Mitochondria are the powerhouses of metaboloepigenetics. Mitochondrial function, and particularly the TCA cycle, provides the intermediate metabolites essential to the generation and modification of epigenetic marks in the nucleus. Histone acetylation by histone acetyltransferases (HATs) is dependent on the availability of acetyl-CoA. On the other hand, histone acetylation can be removed by a class of NAD⁺-dependent histone deacetylases called sirtuins. LSD1 and LSD2 catalyse demethylation of mono- and di-methylated lysine residues using FAD as a cofactor. The availability of α-ketoglutarate (α-KG) influences histone and DNA demethylation by JmjC and TET enzymes respectively. Succinate, fumarate, and 2-hydroxyglutarate (2-HG) can also influence the epigenetic landscape by inhibiting α-KG-dependent histone and DNA demethylation. Ac, acetyl group; Me, methyl group.