How we age gracefully and whether there is anything we can do to slow the process has long fascinated humanity. But despite ongoing research, the answer to how we can successfully fight aging remains unclear.

Now, a new study by scientists from the University of Glasgow in collaboration with the Mayo Clinic in the US reveals some of the biological secrets of the aging process, offering a potential new target for treatment.

The study, “Apoptotic stress induces mtDNA release and drives SASP during aging,” was published at: Nature. He studies why aged and damaged cells cause inflammation and how this process can be stopped to promote healthy aging and even improve the treatment of diseases such as cancer.

As we age, our cells produce inflammatory proteins that further contribute to aging. Cancer treatments trigger the same inflammatory process, damaging cells that can prevent effective treatment for patients.

New research led jointly by Professor Stephen Tate from the School of Cancer Sciences and his team reports an important inflammatory role for mitochondria, the energy-producing organelles of our cells.

Researchers have found that in old cells or after cancer treatment, mitochondria become leaky, releasing DNA that promotes inflammation and, as a result, aging. The team then found that if they could prevent mitochondrial leakage, it inhibited inflammation and improved health during aging.

Their discovery suggests that targeting mitochondria-driven inflammation may offer a new way to promote healthy aging as well as improve response to cancer treatments.

Professor Stephen Tait said: “Our study reveals a completely unexpected link between mitochondria and the inflammatory effects of old cells. We found that mitochondrial permeability, a process originally linked to cell death, promotes inflammation in old and damaged cells. This opens up new avenues for aging and cancer.” “This is research with exciting potential for new treatments.”