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Research Paper Volume 7, Issue 7 pp 486—499

Transgenic mice overexpressing glia maturation factor-β, an oxidative stress inducible gene, show premature aging due to Zmpste24 down-regulation

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Figure 10. Hypothetical schematic representation of the novel role of GMF overexpression in non-brain tissue in vivo.

This study showed that the GMF-TG mice developed accelerated aging phenotypes due to lamin injury caused by oxidative stress-related reduction of Zmpste24. Zmpste24 is down-regulated in response to oxidative stress [19, 20], which appears to be associated with the activation of p53 and p16-Rb pathways [19]. Oxidative stress activates the p53 and p16-Rb pathways, inducing senescence and eventually leading to accelerated aging [22, 23]. It is conceivable that the ectopic GMF overexpression might be a factor connecting aging and lamin injury through oxidative stress.