Senescent cells have removed themselves from normal operation and really should be destroyed, either by their own programmed cell death processes or by the immune system. Senescent cells accumulate with age, however, and while in place cause harm to surrounding tissues. Removing these unwanted and damaging senescent cells with targeted cell killing technologies is one of the necessary goals in longevity science; it has already been shown to provide benefits in gene-engineered mice, and several lines of research are presently leading towards the tools needed to build therapies to attain the same results for everyone else.
Here is another example of the way in which senescent cells are not in good shape:
Parasitic strands of genetic material called transposable elements - transposons - lurk in our chromosomes, poised to wreak genomic havoc. Cells have evolved ways to defend themselves, but in a new study, [researchers] describe how cells lose this ability as they age, possibly resulting in a decline in their function and health.
"The cell really is trying to keep these things quiet and keep these things repressed in its genome. We seem to be barely winning this high-stakes warfare, given that these molecular parasites make up over 40 percent of our genomes." Cells try to clamp down on transposons by winding and packing transposon-rich regions of the genome around little balls of protein called nucleosomes. This confining arrangement is called heterochromatin, and the DNA that is trapped in such a tight heterochromatin prison cannot be transcribed and expressed. What the research revealed, however, is that carefully maintaining a heterochromatin prison system is a younger cell's game. "It's very clear that chromatin changes profoundly with aging."
Young and spry cells distinctly maintain open "euchromatin" formations in regions where essential genes are located and closed "heterochromatin" formations around areas with active transposable elements and few desirable genes. The distinction appeared to become worn in aging, or senescent, cells. In the observations, the chromatin that once was open tended to become more closed and the chromatin that was once closed, tended to become more open. Then the scientists compared the DNA that was coming from open or closed chromatin formations in the young and senescent cells. In their study not only did they find that the chromatin lockdown was breaking down, but also that the newly freed transposons were taking full advantage.
What's not clear from the study is the relevance of the damage that the cells suffer from the transposable element jailbreak and resulting genetic crime spree. "Is the transposition really bad for the organism or is it something that happens so late that by that point the organism has already accumulated so much age-associated damage? Then maybe this extra insult of transposition is not going to make a lot of difference."