Cells become senescent in response to a variety of circumstances. The vast majority are cases of replicative senescence, somatic cells reaching the Hayflick limit. Cell damage and toxic environments also produce senescence, and senescent cells are also created as a part of the wound healing process. A senescent cell ceases replication and begins to secrete inflammatory and pro-growth signals, altering the nearby extracellular matrix and behavior of surrounding cells – even encouraging them to become senescent as well.
Near all senescent cells last a short time only, as they self-destruct or are removed by the immune system. When the presence of senescent cells is transient, their signals are a useful part of the processes of regeneration following injury.
Purple vacutainers for blood testing. Image credit: Amanda Mills, USCDCP, CC0 Public Domain via Pixnio
Cellular senescence also serves to lower the risk of cancer, ensuring that cells with significant DNA damage (or that might gain significant DNA damage due to a locally genotoxic environment) are prevented from replication. Senescent cells linger with age, however. In older tissues they last longer and are created in greater numbers, and their signals become very harmful when present for the long term. In this way, cellular senescence is an important cause of aging.
While compelling evidence has existed for decades for the accumulation of senescent cells to be a contributing cause of aging, this area of study has only comparatively recently found acceptance and significant funding. A decade ago near all work on senescent cells took place in the context of cancer, carried out by researchers who didn't think that senescence was all that relevant to aging at all.
Cancers generate senescent cells by their very nature, and there is a complex relationship between cellular senescence and cancerous tissues. Senescence is an initially protective mechanism when the number of cells (cancerous and senescent) is small, locking down replication and summoning immune cells. Given established cancer tissue, or the burden of senescent cells in old tissues, then the inflammatory, pro-growth signaling of senescent cells instead encourages cancer growth and spread. Some cancers, particularly leukemias, even appear to aggressively generate more senescent cells in order to accelerate their growth.
Link: Bone Marrow Senescence and the Microenvironment of Hematological Malignancies
Source: Fight Aging!