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. 2018 Jul 25;12:196. doi: 10.3389/fncel.2018.00196

Figure 1.

Figure 1

SIRT3 influences oxidative phosphorylation and oxidative stress management. SIRT3 increases ETC efficiency by deacetylating and regulating the activities of mitochondrial complexes I, II, III, IV and V to increase ATP production. SIRT3 reduces mitochondrial oxidative stress directly by deacetylating IDH2 and MnSOD and also increasing GSH levels, and thereby enhancing ROS detoxification. SIRT3 can also negatively regulate ROS levels in some tissues indirectly by upregulating UCP expression, which lessens the driving force for mitochondrial ROS production by decreasing ΔΨm. SIRT3 can also negatively regulate the opening of the mPTP by deacetylating CypD. SIRT3 also orchestrates mitochondria-nuclear cross-talk by deacetylating and activating mitochondrial FOXO3A, which then travels to the nucleus to activate the transcription of anti-oxidative genes, and by indirectly activating the transcription factor CREB, which activates genes whose products play roles in mitochondrial biogenesis. CREB, cAMP response element-binding protein; CypD, cyclophilin D; ETC, electric transport chain; FOXO3a, forkhead box O3; GSH, glutathione; IDH2, isocitrate dehydrogenase; MnSOD, manganese superoxide dismutase; mPTP, mitochondrial permeability transition pore; ROS, reactive oxygen species; UCP, uncoupling protein; ΔΨm, change in mitochondrial membrane potential.