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Aged female mice with skeletal muscle-specific deletion of Terf2, which encodes the telomere-protective factor TRF2, display a remarkably young-like muscle phenotype including reduced myofibre atrophy, preserved muscle strength, absence of regenerative nuclear markers and modest lifespan extension. This phenotype occurs without evidence of telomere deprotection but is associated with mild pro-oxidant signalling; hence, we propose that age-associated TRF2 downregulation induces a hormetic response that benefits skeletal muscle function during ageing. This article is part of the theme issue 'Developmental circuits in ageing'.
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Gilson et al. (2026) studied this question.
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