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. 2021 Feb 4;21(4):258. doi: 10.3892/ol.2021.12519

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Copyright: © Mukherjee et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 3. — Pathological and physiological significance of ERRα. (A) Regulation of mitochondrial energy production and oxidative phosphorylation, hepatic metabolism of glucose and lipids, distinctive control of type 2 diabetes in liver and skeletal muscles and implication as potential therapeutic target in the treatment of glucose excess, obesity and diabetes. (B) Significance of ERRs mediated signaling control in Krebs (TCA) cycle and oxidative phosphorylation, in which ERRα and ERRγ isoforms serve as central regulatory pillars of metabolic genes and cellular energy metabolism. ERRβ,has been reported to be vital for maintenance of embryonic stem cell pluripotency (110). MDH, malate dehydrogenase; FH, fumarate hydratase; SDH, succinate dehydrogenase; ACO2, aconitase hydratase; IDH3, isocitrate dehydrogenase; DLD, dehydrogenase complex; PDH, pyruvate dehydrogenase; SUCLG1, succinyl-Coenzyme A ligase; GOT1, aspartate aminotransferase, cytoplasmic; GOT2, aspartate aminotransferase, mitochondrial; CS, citrate synthase; ERR, estrogen related receptor; NSCLC, non-small cell lung cancer; ATP, adenosine triphosphate dihydrolipoamide dehydrogenase; DLAT, dihydrolipoyl transacetylase; OGDH, oxaglutarate.