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Interestingly, while Mlkl / and Mlkl AA mice showed high protection against AAA development, Ripk1 D138N/D138N mice were only partially protected from aortic dilation compared to WT mice, indicating that AAA formation is in part independent of RIPK1-induced apoptosis

Interventions that slow or reduce cellular senescence including telomere maintenance address this mechanism at its source

Garolla et al

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In summary, our results provide clear evidence for the role of C32E8.9 in lifespan extension resulting from impaired mitochondrial translation by modulating innate immunity and lipid reprogramming