Senescence is a cellular response characterised by morphological changes, a stable growth arrest (in order to prevent tumoral proliferation) and a change in the cell’s secretome.
Indeed, senescent cells, called Zombie cells, produce a large amount of senescence-associated secretory phenotype (SASP) which is responsible for a pro-inflammatory response, for collagen degradation, for free radical production, and for the transmission of the senescent state.1 As a result, senescent cells tend to accumulate with age and 20 to 60% of the skin cells are actually senescent.2
The senescence process may be induced by several causes. Ageing is the most common phenomenon (after a certain number of division, a cell may go into senescence), but another frequent cause is stress, especially oxidative stress that induces inflammation. The combination of ageing and moderated inflammation caused by stress is called inflamm’aging, also known as “secret killer”. This progressive and insidious phenomenon has visible effects in the long term and prevents the skin from ageing well.
When a cell is exposed to stress, there are a few possible outcomes. It can be repaired, it can undergo apoptosis (the programme cell death) if it is too severely damaged, or it can undergo senescence.
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