Cellular senescence is the phenomenon by which normal diploid cells lose the ability to divide, normally after about 50 cell divisions in vitro. Some cells become senescent after fewer replication cycles as a result of DNA double strand breaks, toxins, etc. This phenomenon is also known as "replicative senescence", the "Hayflick phenomenon", or the Hayflick limit in honour of Dr. Leonard Hayflick, co-author with Paul Moorhead, of the first paper describing it in 1961. In response to DNA damage (including shortened telomeres), cells either age or self-destruct (apoptosis, programmed cell death) if the damage cannot be easily repaired. In this 'cellular suicide', the death of one cell, or more, may benefit the organism as a whole. For example, in plants the death of the water-conducting xylem cells (tracheids and vessel elements) allows the cells to function more efficiently and so deliver water to the upper parts of a plant. The ones that do not self-destruct remain until destroyed by outside forces. In a study conducted in 2011 on mice, senescent cells were deliberately eradicated, which led to greater resistance against aging-associated diseases. Cellular senescence is causally implicated in generating age-related phenotypes, and removal of senescent cells can prevent or delay tissue dysfunction and extend healthspan.
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