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Therefore, revealing the crosstalk and additional key regulators of oxidative cell death pathways is crucial for identifying new targets for drug development and screening

doi: 10.1016/j.cell.2007.09.018 183 KronfolZ.RemickD

f , Sunburst plot of differentially expressed genes belonging to biological process functional terms computed with SynGO

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demonstrated in mice that chronic inflammation, induced by the knockout of the nfkb1 subunit of the NF-B transcription factor, exacerbates telomere dysfunction and cell senescence through a feedback loop involving NF-B, COX-2, and ROS, thereby leading to premature aging and reduced tissue regeneration in liver and gut (Jurk et al., 2014)

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