A dominant principle underpinning our understanding of the ageing process is that DNA damage induces a stress response that shifts cellular resources from growth towards maintenance. A contrasting and seemingly irreconcilable view is that prompting growth of, for example skeletal muscle, results in systemic benefit. To investigate the robustness of these axioms, we induced muscle growth in a murine progeric model. Here we show that the muscle of Ercc1Δ/- progeric mice undergoes an extremely severe form of wasting which can be protected through an intervention that attenuates myostatin/activin signalling.

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