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Mitochondrial dysfunction and oxidative stress are increasingly appreciated as important players in cardiovascular and metabolic diseases, including insulin resistance and atherosclerosis. Therefore, improving cardiac mitochondrial and redox function may be a promising therapeutic strategy in such pathologies. One exciting candidate is coenzyme Q or CoQ, an essential redox-active lipid crucial for ATP production and antioxidant defence. Key studies have demonstrated that CoQ is decreased in insulin resistance and atherosclerosis, and ‘industrial’ amounts of supplemental CoQ inhibit both diseases in pre-clinical models. Therefore, restoring normal mitochondrial concentrations of CoQ is an obvious target to potentially ameliorate a range of cardiovascular and metabolic diseases.

We have recently identified 30 novel CoQ regulatory genes in a yeast screen, including phosphatidylethanolamine methyltransferase (PEMT). Decreasing PEMT effectively increases mitochondrial CoQ in yeast, mammalian cells and lab models. Moreover, increasing mitochondrial CoQ via PEMT blockade protects against insulin resistance, thereby establishing the potential utility of this approach to treat diseases of mitochondrial CoQ deficiency. Our data indicates that PEMT deficiency alters mitochondrial SAM/SAH content and this is key in driving increased CoQ biosynthesis. We hypothesise that PEMT AND the molecular processes underlying PEMT deficiency (eg, mitochondrial SAM/SAH content) could represent novel therapeutic targets to alter cellular CoQ content and treat disease in humans.

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