Cellular senescence, oxidative stress, and mitochondrial dysfunction are common aging-related processes that exacerbate the neurodegenerative pathways in both diseases [8, 9]
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For instance, recent studies indicate that GPX4 stability is regulated by the ubiquitin-proteasome pathway, where its protein may be recognized and degraded by specific E3 ubiquitin ligases
In our study, we demonstrated a persistent senescent-inflammatory microenvironment and a p53-serine 15 phosphorylation regulatory mechanism in keloids, which may play crucial roles in the aggression and recurrence of keloids