Towards an Understanding of How Cellular Senescence Spreads
In its role as an adaptation to suppress cancer, it makes sense that cellular senescence can to some degree spread through a cell population, as well as alter the behavior of surrounding cells in other ways. After all if one cell in a tissue is at risk of cancer, then it is likely others will also be under threat. So the more senescent cells there are, there more likely it is that nearby cells will also become senescent. This is driven by what is called senescence-associated secretory phenotype (SASP) - the particular combination of signaling and other proteins emitted by senescent cells.
This would all be fine and well, but the presence of senescent cells harms tissue integrity and causes other forms of dysfunction that contribute to the advance of degenerative aging. The immune system does work to destroy these cells, but falls down badly on that job in later life: senescent cells accumulate and cause great harm. Ideally we'd want to destroy them all and management of cancer suppression and treatment through medical technology, thus having the best of both worlds. This approach lies near in the future: almost all of the necessary pieces already exist, and it is just a matter of marrying some form of targeted cell destruction technology of the sort developed for use as a cancer therapy with some way of reliably detecting senescent cells based on their distinctive biochemistry.
Here researchers are looking at SASP in more detail, to see how it impacts the ability of one stem cell population to do its job of tissue maintenance:
Cellular senescence is the permanent arrest of cell cycle, physiologically related to aging and aging-associated diseases. Senescence is also recognized as a mechanism for limiting the regenerative potential of stem cells and to protect cells from cancer development. The senescence program is realized through autocrine/paracrine pathways based on the activation of a peculiar senescence-associated secretory phenotype (SASP).We show here that conditioned media (CM) of senescent mesenchymal stem cells (MSCs) contain a set of secreted factors that are able to induce a full senescence response in young cells. To delineate a hallmark of stem cells SASP, we have characterized the factors secreted by senescent MSC identifying insulin-like growth factor binding proteins 4 and 7 (IGFBP4 and IGFBP7) as key components needed for triggering senescence in young MSC.
These results suggest the occurrence of novel-secreted factors regulating MSC cellular senescence of potential importance for regenerative medicine and cancer therapy. [We] believe that our results pave the way to further investigations aiming to modify, in the near future, the current in vitro MSC expansion protocols for therapeutic purposes, thereby preventing or reducing the occurrence of negative senescence-related effects, and to better understand the complex process of senescence and aging in stem cells.
I've wondered for some time why cells go to the bother of cell cycle arrest versus activating apoptosis. The latter pathway is far cleaner and less destructive to surrounding tissue, so it is reasonable to expect apoptosis would be selected over senescence.
I imagine it's probably a case of it being easier to just get a cell to stop dividing rather than go to that extra step of killing it. Evolution is extremely sloppy, and given that it takes until after most reproduction has been done for senescent cells to accumulate to harmful levels, there likely isn't much selective pressure for doing a more thorough job.
@Arcanyn I'd speculate (as I think Reason is above) that senescent cells are the body's equivalent of robbing peter to pay paul. A short term solution that creates bigger problems in the medium term.
Perhaps in youth senescent cells help to deal with potential cancerous cells by turning an area senescent, which the immune system then kills (the immune system also directly kills cancerous cells). As the immune system ages, it no longer kills senescent cells or cancerous cells, but cells turning senescent is still an advantage as it suppresses cancer in the short term, at the expense of causing more cancer in the medium term. But if an animals immune system has already aged, then in the wild it probably doesn't have that much longer to live anyway as it is already old, so evolution selects for damaging senescence as a short term benefit.