When the Iron Rations are Rusting: Aging Stem Cells
Many cells in the human body are able to divide themselves, thus helping tissues and organs to regenerate, e.g. if wounds are healing. But this regenerative capability is limited.
One reason for the shrinking regeneration in age is that our stem cells – so-to-speak the mother cells of all types of cells – olden as well. To defend our DNA from damages due to cell division, it owns specialized protective caps, so-called telomeres that shorten with every cell division. Enzyme Telomerase is in charge of renewing these protective caps – but only for certain cell types. For all others, genetic information is lost or damaged when after a certain number of cell divisions the telomeres are gone, leading to cell death (and, thus, to organ dysfunctions) or to the proliferation of “wrong” cells, which in consequence may lead to cancer.
Many stem cells try to avoid these damages by “sleeping”. They stay in the so-called state of “quiescence” and are only activated in case of severe tissue injury when a strong regeneration is needed. After they finished their work (dividing into several sub-types of cells needed to repair and maintain a tissue), they go back to sleep. Like that, their telomeres are protected from shortening.
But in age, this falling-back into dormancy periods is disturbed leading to a permanent activation of stem cells and, thus, to the depletion of our genetic reserves. In the end, also in these senescent stem cells cell division is disturbed or altered cells can proliferate.