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Multiple mechanisms drive pathological ROS accumulation in diabetic cardiomyocytes, such as inhibition of mitochondrial oxidative phosphorylation elevating O 2 production, activation of NOX by angiotensin II (Ang II) and TNF-, and AGEs-RAGE binding-induced NF-B activation that triggers inflammation and further ROS generation

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159,160 GHD1 shRNA has no effect on PDAC cells growth, while knocking down GOT2 elevates ROS levels and leads to cell senescence

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