Controlling "inflammaging"

Absolutely. Aging is accompanied by a decline in general health, a decrease in normal organ function and an increased risk of developing diseases such as cancer, atherosclerosis, diabetes and Alzheimer's. All of this is related to a chronic low-level inflammation that we call “Inflammaging”. We know that the accumulation of so-called senescent cells – damaged cells that are no longer able to proliferate or perform their functions properly but remain alive and active in the body – is at least partly responsible for these problems.

That's right. The negative effects of senescent cells are mainly due to the production of a multitude of pro-inflammatory molecules. So, it goes without saying that targeting and manipulating their inflammation or simply eliminating senescent cells would offer hope for new therapeutic approaches to “cure” the negative aspects of aging and associated pathologies. Understanding the mechanisms controlling this inflammation therefore seems essential to refine emerging therapeutic approaches that seek to improve healthspan during aging through the manipulation of cell senescence.

We have discovered a new mechanism to control the pro-inflammatory aspect of senescent cells. More specifically, we have highlighted a new protein function for the MRE11 and ATM proteins, which are already known for their absolutely essential role in DNA repair. Removing or inhibiting these proteins prevents the production of pro-inflammatory molecules by senescent cells. Our study provides answers to questions that have been left unanswered for nearly 10 years and opens up very interesting prospects for further research. Very often, finding the answer leads to new questions. In this case, we must now find a way to interfere with the pro-inflammatory aspect of these proteins without preventing them from repairing the DNA properly. According to our results, this seems possible, so the avenues of research have already been mapped out.