What is the difference between cell division and cellular ageing?

Every cell in your body can only divide a limited number of times. That number is called the Hayflick limit, and human cells reach that threshold after dozens of rounds of division. After that, they stop dividing but do not die: they remain active, send out signals and influence their surroundings. This stage is called senescence, or cellular ageing. Cell division is therefore the process; senescence is what comes after it.

The connecting link between the two is the length of telomeres: the protective end caps of chromosomes. With each division they become slightly shorter. When they become critically short, the cell triggers an internal alarm. The result is senescence or cell death. Telomere shortening is therefore the molecular bridge between how many times a cell has divided and how 'old' it has become. Greater telomere shortening over a lifetime is associated with earlier mortality and more age-related diseases. At the same time, telomere maintenance has a downside: genetic variations in it can raise or lower the risk of certain cancers, depending on the type.

Not all cell division is equal. In some cells, ageing factors are distributed unequally between the two daughter cells during division. That may sound like an error, but it can actually be protective: one daughter cell inherits the damage, while the other starts out cleaner. Disruptions to this mechanism can accelerate ageing.

Ageing is, incidentally, broader than cell division alone. In cells from worms, flies, mice and humans, the rate at which genes are read to produce proteins speeds up with age. That acceleration comes at the cost of accuracy: more errors creep into proteins, independent of how many times the cell has divided. Slowing down this reading process has been shown to extend the lifespan of laboratory animals. Cellular ageing is therefore not simply a matter of having divided too many times.