Age-associated degeneration is caused, at least in part, by accumulated cellular damage, including DNA damage, but how these types of damage drive aging remains unclear. Dr. Paul Robbins and colleagues at the University of Pittsburgh sought to address this question using a mouse model of DNA repair deficiency. The Robbins team found that DNA damage drives aging, in part, by activating NF-κB, a transcription factor that responds to cellular damage and stress. They report that inhibition of NF-κB reduces oxidative stress, oxidative DNA damage, oxidative protein damage, and cellular senescence induced by oxidative damage. Their data suggest that NF-κB inhibitors can mitigate cellular damage and could provide clinical benefit for degenerative changes caused by aging.
NF-κB inhibition delays DNA damage-induced senescence and aging in mice
University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
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