Cells become senescent after many divisions or after suffering some forms of damage. They cease dividing and leave the cell cycle. Most are destroyed, either by the mechanisms of programmed cell death or by the immune system, but unfortunately some remain, and their numbers grow with time. The presence of senescent cells harms surrounding tissues, and the more senescent cells that exist the greater the harm. In this, cellular senescence - or rather the accumulation of senescent cells - is one of the root causes of degenerative aging.

What to do about this? Much of the past discussion here at Fight Aging! has focused on efforts to destroy senescent cells - to pick up the slack and eliminate those senescent cells overlooked by existing mechanisms in our biology. Periodically sweeping these cells from the body should prevent their accumulation from ever reaching damaging levels. See those posts from the archives, for example:

• A Demonstration of the Merits of ApoptoSENS
• Needed: a Robust Way of Identifying Senescent Cells
• A Way to Target Senescent Cells

Destruction is one approach, but there is another: researchers could seek a practical way to reverse cell senescence. I would be the first to suggest that this will prove far more challenging than simply destroying the errant cells, but there are some hints that researchers might have to do this for at least some of the cells in the brain. If a significant portion of the neurons that store the data of the mind become senescent, then we can't just forge ahead with global destruction of everything that looks like a senescent cell.

So how do you go about rescuing a senescent cell, and more importantly do so in a way that can be undertaking in a living body rather than only in a petri dish cell culture? Here is a paper that looks at the senescent cell issue in aging from this perspective:

Rejuvenation of senescent cells - the road to postponing human aging and age-related disease?

Senescent cells characterized by the presence of [various senescence markers] accumulate in tissues of aged animals and humans as well as at sites of pathology. It is believed that cellular senescence evolved as a cancer barrier since non-proliferating senescent cells cannot be transformed to neoplastic cells. On the other hand senescent cells favor cancer development, just like other age-related pathologies, by creating a low grade inflammatory state due to senescence associated secretory phenotype (SASP).

Reversal/inhibition of cellular senescence could prolong healthy life span, thus many attempts have been undertaken to influence cellular senescence. The two main approaches are genetic and pharmacological/nutritional modification of cell fate. The first one concerns cell reprogramming by induced pluripotent stem cells (iPSCs), which in vitro is effective even in cells undergoing senescence, or derived from very old or progeroid patients. The second approach concerns modification of senescence signaling pathways just like TOR-induced by pharmacological or with natural agents.

However, knowing that aging is unavoidable we cannot expect its elimination, but prolonging healthy life span is a goal worth serious consideration.

 

If you watch the field for long enough, you gain a certain sense for sentences that were added to appease conservative funding sources or elder laboratory peers, and that last line above is a classic of the type. For a long time it was very harmful to future career prospects in the field to talk openly about therapies for aging, and while that is far from the case today, some remnants of that former wall of silence remain. That it existed at all is unconscionable - exactly as though the cancer research community or other major part of the medical science establishment did nothing but watch and calibrate the degree of pain, suffering and death caused, rather than try to work towards cures.

The processes of aging are unavoidable in our present biology - but that says nothing about how well we can intervene. The processes of rust are unavoidable in cars, but if you maintain a car well enough it can last indefinitely. The same principle applies in the engineering of greater longevity for living organisms: the regular application of therapies to repair the forms of cellular and molecular damage that cause aging, thereby keeping its consequences at bay for so long as those therapies are continued. That is the intermediate term goal for biotechnology and medicine.