What are senescent cells and why are they bad for you?
Senescent cells are damaged cells that stop dividing but continue to live and chronically inflame their surroundings. They accumulate as you age and are strongly linked to age-related diseases, but because they also play a protective role, simply clearing them all away is not an option.
Every cell in your body has an emergency brake: if it sustains too much damage, it can permanently stop dividing. Those are senescent cells. They no longer respond to growth signals, and they do not die off in the normal way either. That combination, being permanently halted yet continuing to live, is what makes them remarkable.
Cells enter this state because of DNA damage, because of telomere shortening (the protective caps at the ends of your chromosomes become a little shorter with every cell division), or because a gene that can cause cancer suddenly switches on. It is therefore an emergency response to a threat. In the short term that is clever: a damaged cell that stops dividing cannot form a tumour.
The problem starts when those cells accumulate. Senescent cells secrete large quantities of inflammatory substances, a mixture of signalling molecules, enzymes and other compounds that stir up their surroundings. This produces a smouldering, chronic inflammation that persists for years. Research links that accumulation to atherosclerosis, osteoarthritis, chronic lung disease and an increased cancer risk. Whether this is always directly the cause in humans or is partly a consequence as well has not yet been fully resolved, but the evidence is strong.
Senescent cells also actively survive: they switch on protective mechanisms that prevent them from dying, even when they carry considerable damage. That makes them stubborn. In the brain they accumulate with ageing and in diseases such as Alzheimer's, but there the causal role is still unclear.
Yet senescence is not a purely bad thing. During embryonic development and during tissue repair after injury, senescent cells play a useful role, and they also form a barrier against cancer. This makes it difficult to simply clear them all away: too little senescence can lower the threshold for cancer. Treatments that target senescent cells specifically are being actively developed, but are not yet part of everyday clinical practice.
Based on multiple reviews and mechanistic studies (PMID: 30648461, 29477613, 33328614, 32800277, 35015337, 36732079, 38583577, 38030088). The causal evidence in humans is strongly plausible for most age-related diseases but has not yet been fully proven through interventions in humans. The brain findings are preliminary and associative.