As johnswentworth recounts in Core Pathways of Aging, as an organism ages active transposons within it's stem cells duplicate and that mechanism might lead to increased average transposons count in stem cells. Those transposons then produce DNA damage which in turn leads to cell senescence.
If that hypothesis is true, there's evolutionary pressure to keep the count of active transposons low. That evolutionary pressure is greater in organism that reproduce at a later age then for organisms that reproduce at an earlier age.
As Bret Weinstein describes, breeding protocols for lab mice have lab mice reproducing at an earlier age then mice that live in the wild because it's economical to make the mice reproduce at a young age. Weinstein made the hypothesis that this leads to laboratory mice having elongated telomeres.
I hereby make the hypothesis that if we investigate the average amount of active transposons in laboratory mice and lab mice, we will find that the wild mice have less active transposons then the wild mice, because there's less evolutionary pressure in the laboratory mice to remove mutations that lead to increased active transposon count.
If investigation finds this hypothesis to be true, approaches to reduce transposon count should get more attention by antiaging researchers.