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Targeting aging: lessons learned from immunometabolism and cellular senescence

The second is the inflammation-apoptosis dual inhibition barrier: blocking the NF-B/p38-MAPK/COX-2/iNOS inflammatory cascade, attenuating the inflammatory response through the dual regulation of STAT3/STAT1 and inhibiting the JNK/p53-mediated pro-apoptotic signaling and regulating the balance of Bcl-2/Bax/caspase-3, which is the most effective way to reduce the inflammatory response in mitochondria and ferroptosis