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We propose that rather than viewing these as a stochastic event, the underlying biology that is challenged over time in certain cell types contributes to non-protective senescence mechanisms, failed resilience (mitochondrial guarded), and ultimately chronic lung disease

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In this situation, the prototypical pathway is based on the interaction of TNF family members with specific ligands, the recruitment of receptor-interacting protein kinase 1, the inhibition of caspase 8, the assembly of the RIP1/RIP3 signaling complex, and the formation of the necrosome

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