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Rejuvenation

Will Drugs Targeting Senescent Cells Deliver?

Posted on 2 March 2020

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As we age, an increasing number of our cells will enter an inactive state called senescence. Senescent cells no longer divide, and release signals that contribute to tissue dysfunction. Various factors can drive cells into senescence, such as telomere shortening and damage from inflammation and oxidative stress.

McHugh, D., & Gil, J. (2017). Senescence and aging: Causes, consequences, and therapeutic avenues. The Journal Of Cell Biology217(1), 65-77. doi: 10.1083/jcb.201708092

The immune system usually removes senescent cells. However, once they accumulate in sufficient numbers, the signals released by senescent cells interfere with the immune system’s ability to remove them.

Enter senolytics: drugs designed to target senescent cells and the networks that sustain them, with the hope of slowing the ageing process. Development of such drugs began in the mid 2000s, but we are only just now beginning to see senolytic therapies tested in small human clinical trials. The results so far are promising: senolytics appear capable of reducing senescent cell burden, and can improve symptoms in diseases in which senescent cells play a significant role.

Excitement over senolytics could still be premature, however. Trials have so far been limited to patients with severe senescence-associated pathologies. It remains to be seen whether senolytics will slow age related decline in healthy individuals. Furthermore, senolytics could have serious side effects that have not yet been picked up in the small clinical trials. There is now concern that senolytics may be sold and used for self-medication before their safety can be rigorously tested.

A formula claiming rejuvinating effects currently being sold
Senolytic Complex. (2020). Retrieved 2 March 2020, from https://us.supersmart.com/en–anti-ageing–senolytic-complex–0781

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    References

    Discovery, Development, and Future Application of Senolytics: Theories and Predictions: https://doi.org/10.1111/febs.15264

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