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Considering that metformin-induced mitochondrial complex I inhibition impairs NADH oxidation and elevates NADH levels, these transcriptional changes probably represent a compensatory adaptation to restore redox homeostasis by enhancing NADPH generation

This process aids glucose regulation

Therefore, use of rhEPO for treatment of tissue injury is limited by the potential side effects of increased erythrocyte mass and endothelial cell activation, which, in combination with activated platelet production, predisposes to thrombosis (6,7)