While specific transposons are integrated functional components of host biology, most mammalian transposons are potentially detrimental to the host genomes, thus inactivated via degenerative mutations and/or transcriptional/post-transcriptional silencing. Interestingly, aberrant transposon induction has been observed in a variety of pathological conditions, including aging, cancer and infection. We aim to investigate the mechanism underlying transposon dysregulation during reproductive aging and to elucidate the effects of transposon-host interactions on cellular processes that accelerate aging.