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The suppression of PGC-1α due to a deficit of endothelial nitric oxide synthase can lead to drastic decreases in activities of mitochondrial antioxidant enzymes (Weinberg, 2011)

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ROS play important roles at the ER, where their production activates the unfolded protein response (UPR), accompanied by the inactivating sulfhydration of protein tyrosine phosphatase 1B (PTP1B) that results in the increased phosphorylation and, hence, activation of PERK 91