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