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This degradation, in turn, allows NF-B activity to increase, resulting in increased transcription of pro-inflammatory genes, including TNF-, IL-1, IL-6, and inducible nitric oxide synthase (iNOS) (Morgan and Liu, 2011)

Chronic treatment with N-acetyl-cystein delays cellular senescence in endothelial cells isolated from a subgroup of atherosclerotic patients

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The less mature immune system observed in neonates enables a more balanced regenerative reaction within the mammalian heart through activating cardiomyocyte proliferation and angiogenesis via interleukin-6/signal transducer and activator of transcription signaling 41,42

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