Changes in the Senescence-Associated Secretory Phenotype or Failing Immune Surveillance?

Cells can become senescent in reaction to a variety of environmental stresses or forms of damage, activating a program that halts cellular replication and triggers the generation of a mix of potent signals that can influence surrounding cells and tissue structure, a state known as the senescence-associated secretory phenotype (SASP). Senescent cells have a role in embryonic development, controlling the shaping of tissues at the extremities, such as the growth of fingers. Their existence in adults is perhaps because the same mechanism, particularly the arrested growth aspect of it, serves to suppress cancer risk - or at least it does so initially and while senescent cells are present in only modest numbers. Evolution tends to lead to complex systems in which every component part is reused in many ways. Among the signals making up SASP there are those that encourage the immune system to destroy senescent cells, should those cells fail to trigger their own programmed cell death processes. The immune system has its own issues that manifest during the aging process, however, and it becomes ever less effective at all of its tasks, whether that is protecting the body from invading pathogens or destroying unwanted and potentially dangerous native cells. Over a lifetime ever more of the cells in our tissues become senescent and linger rather than being cleared out. Their collective SASP grows in influence, degrading tissue function and contributing greatly to age-related frailty and ...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs