Does chronic inflammation accelerate the ageing of your cells?

Chronic low-grade inflammation does indeed accelerate cellular ageing, and it does so through a self-reinforcing cycle. Cells that have been damaged stop dividing but do not die: they become 'senescent' (aged) and secrete a package of inflammatory substances. Those substances in turn cause surrounding healthy cells to age rapidly, while at the same time weakening the immune system so that the senescent cells are cleared away less effectively. The more senescent cells accumulate, the more inflammation there is, and the more inflammation there is, the faster cells age.

The consequences extend beyond cell biology. In joints, those inflammatory substances contribute to joint destruction, which neatly explains why osteoarthritis is a disease of old age. In the skin, senescent connective-tissue cells accumulate and break down collagen, leading to wrinkles and thinner skin. There is also a link with the brain and with type 2 diabetes, but the precise contribution of cellular ageing to each condition has not yet been established equally precisely for every disease.

Cellular ageing is, incidentally, not purely negative. It is also a built-in protective mechanism: by stopping dividing, a damaged cell prevents itself from growing into a cancerous tumour. It is only when senescent cells accumulate en masse and continue to secrete inflammatory substances over a prolonged period that this protective mechanism turns into something harmful. That makes intervening in this system, for example with so-called senolytic agents that clear away senescent cells, a much-discussed but complex challenge.

One potential point of intervention is a protective system within cells that counteracts oxidative stress and dampens inflammatory processes. This system weakens with age, which accelerates the vicious cycle. Activating it reduced the number of senescent cells and their associated inflammatory substances in laboratory studies. Whether this also works clinically in humans has not yet been sufficiently investigated. There are therefore concrete molecular targets in view, but proven therapies do not yet exist.