Researchers have discovered a key molecular process that may contribute to chronic inflammation as we age. If this process can be accurately targeted, it could unlock ways to stay healthier in our later years.

The discovery centers on the unique strands of DNA contained within our mitochondria, the power stations of our cells. By banishing their 'mtDNA' into the surrounding cytoplasm, mitochondria can cause inflammation. Yet just how or why this happens has never been well understood.

In this study, researchers led by a team from the Max Planck Institute for Biology of Ageing in Germany analyzed tissue samples from humans and test animals, using mice genetically engineered to be models of aging and disease.

They found that when mtDNA can't find enough DNA building blocks (deoxyribonucleotides) for replication, it picks up RNA building blocks (ribonucleotides) instead. This mistake in construction causes instability in the mtDNA, which leads to it being ejected from the organelle.

"Our findings explain on a molecular level how metabolic disturbances can lead to inflammation in senescent cells and in aged tissue and open up new strategies for possible interventions," says molecular biologist Thomas Langer, from the Max Planck Institute for Biology of Ageing.