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[130] suggested MT-1 and MT-2 as novel therapeutic targets against diabetic nephropathy, as the expression of these genes was increased by high glucoseinduced oxidative stress in renal proximal tubular epithelial cells

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In addition, PARP-1 and AMP-activated protein kinase (AMPK) mutually reinforce each other: The activation of PARP-1 stimulates AMPK, which in turn phosphorylates and activates PARP-1

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