Inside our bodies, a damaged cell may stop dividing without dying. Instead, it remains active and continues communicating with surrounding cells. Why does the body retain such a cell, and when does its continued presence become a problem?
اضافة اعلان
This condition is known as cellular senescence: a stable state in which a cell stops dividing and undergoes changes in its activity and functions. The cell does not necessarily have to be chronologically old to enter this state. It may do so in response to DNA damage or signals that push it toward abnormal division.
In such cases, cell-cycle control pathways involving proteins such as p53 and p16 are activated, limiting further proliferation. The benefit is clear: damaged cells are prevented from producing more cells carrying the same defects, making this response one of the key barriers against tumour development.
However, stopping cell division does not stop everything the cell does. Senescent cells may begin releasing a mixture of inflammatory molecules, growth factors and enzymes that affect their surroundings. This pattern is known as the senescence-associated secretory phenotype (SASP).
SASP is not a single substance, but a collection of secretions that vary depending on the cell and the surrounding conditions. These molecules can alter the behaviour of neighbouring cells. When their activity persists for a long time, they may contribute to an inflammatory environment and disrupt tissue function. Cell experiments have even shown that some of these secretions can promote behaviours associated with tumour progression in neighbouring cells.
Here lies the paradox: the cell itself stops multiplying, yet its harmful effects on its surroundings may continue. Is it merely a sign of ageing, or does it actively contribute to the ageing process?
To investigate this, researchers conducted a study published in the medical journal Nature in 2016 using mice with a genetic system that allowed them to eliminate targeted cells expressing the p16 protein. The intervention began when the mice were one year old, and the researchers followed their progress in comparison with control groups.
The results showed an increase in median lifespan, delayed tumour development and a reduction in some signs of deterioration in the kidneys, heart and fatty tissue.
The experiment did not rejuvenate senescent cells; it removed some of them. This supports the idea that these cells contribute to age-related damage.
However, eliminating all senescent cells is neither a straightforward nor a guaranteed solution. These cells also serve beneficial functions, including contributing to wound healing. Moreover, p16 is not an exclusive or comprehensive marker of senescent cells, and experiments in mice do not yet establish the effectiveness or safety of this approach in humans.
The more precise research question today is therefore: Which cells cause harm when they persist, and when can they be targeted without disrupting their beneficial functions?
Cellular senescence reminds us that the effects of a protective response can change over time and depending on the circumstances. Understanding this shift is the necessary first step before attempting any medical intervention.
By pharmacist Ibrahim Ali Abu Rumman
