As the research and development community devotes ever greater resources to the development of senolytic rejuvenation therapies based on selective destruction of senescent cells, further exploration of the biochemistry of senescence continues apace. In this example, researchers find that the sirtuin SIRT7 has a role in suppressing cellular senescence that results from certain forms of DNA damage, and speculate that this might explain some of the reports linking SIRT7 activity to aging. As such an early stage of investigation, it is hard to say whether this will become relevant to some form of therapy, however.
Cellular senescence is a state of permanent cell cycle arrest that is induced by diverse types of stress associated with oncogene activation, DNA damage, or chromatin deregulation and can have tumor-suppressive effects. However, senescent cells also have profound deleterious effects that enhance tumor malignancy or contribute to tissue dysfunction in aging and disease. Indeed, senescent cells undergo dramatic alterations in metabolic and gene expression profiles with acquisition of a senescence-associated secretory phenotype (SASP). Through the SASP, even relatively low levels of senescent cells can have far-ranging effects that influence tissue function.