To investigate the effects of the systemic increase in Ccl2 expression on progeria-induced metabolic derangement and lifespan, we generated an experimental model by crossbreeding mice that overexpress Ccl2 [20] with mice bearing a mutation in exon 11 of the lamin A gene (Lmna) to obtain offspring that recapitulate most of the clinical features of Hutchinson-Gilford progeria syndrome in humans (HPGS) [21–23]. This evidence concerns the gene CCL2 and Hutchinson-Gilford progeria syndrome.