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found that GCV and ABT263 improved endothelial function via increased nitric oxide bioavailability and reduced oxidative stress [85]
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Considering that the TNF-α-induced H 2 O 2 burst has been previously shown to cause oxidative inactivation of JNK phosphatases 54 , JNK hyperactivation is a result of the dual action of GPx1 in regulating H 2 O 2 , which leads to activated ASK1 and inactivated JNK phosphatase
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