Senescence-inhibitory Δ133p53α counteracts accelerated ageing and mortality.

ABSTRACT: Research on progeria not only contributes to treatments for the disease but also enhances our understanding of physiological ageing¹. Mouse models of progeria recapitulate pathological ageing phenotypes seen in patients, including cardiovascular defects, increased cellular senescence, systemic inflammation, DNA damage accumulation, and shortened lifespan². In cultured cells from Hutchinson-Gilford progeria syndrome (HGPS) patients, the human p53 isoform Δ133p53α was previously shown to inhibit p53-mediated cellular senescence, proinflammatory IL-6 production, and DNA damage accumulation, and to extend cellular replicative lifespan³. Here we show that, in a heterozygous HGPS mouse model⁴, transgenic expression of Δ133p53α reproduces these in vi

SUBMITTER: Yamada L 

PROVIDER: S-EPMC12776339 | biostudies-literature | 2026 Feb

REPOSITORIES: biostudies-literature