Cellular senescence is one of the causes of aging. Cells become senescent in response to a variety of circumstances, the most common of which is when a somatic cell reaches the Hayflick limit on replication. Senescence also arises as a result of damage, to shut down cells that might become cancerous. Senescent cells cease to replicate, issue inflammatory signals that attract immune cells to destroy them, and usually self-destruct via programmed cell death mechanisms in any case. The problem with cellular senescence arises from the tiny fraction of senescent cells that evade destruction and linger, polluting surrounding tissue with inflammatory and other signals that evolved for short-term benefit only. When present over the long term, the signals secreted by even a comparatively small number of senescent cells will significantly degrade tissue structure and function, disrupt regeneration, and product chronic inflammation. This accelerates the development and progression of near all common age-related diseases.
The targeted destruction of senescent cells has been well proven as a rejuvenation therapy in mice in recent years, and human trials are underway for the first senolytic drugs capable of achieving this goal.