cGAS inhibition reduces cellular senescence without extending lifespan

Researchers have discovered that disabling the protein cGAS in a short-lived fish species inhibits the progression of cellular ageing. This protein plays a role in detecting DNA in unwanted places within the cell, which contributes to chronic inflammation commonly associated with ageing. By disabling cGAS, this cellular ageing decreased, but it had no effect on the overall lifespan of the fish.

cGAS works in two ways in the body. On the one hand, it activates an inflammatory response when there is damage or abnormalities in cells, which is important for repair. On the other hand, it can influence how DNA damage is handled, which is sometimes detrimental to the health of older cells. Completely switching off cGAS therefore also proved to have disadvantages, because it disrupts useful functions.

Variations in cGAS are also known in other animal species and humans that can determine how the body regulates ageing and inflammation. Some variants improve DNA repair, which can be beneficial for healthy ageing. Even so, it is difficult to selectively influence cGAS, as it is involved in both harmful and protective processes.

This research underlines the importance of finding a balance in anti-inflammation during ageing. Chronic inflammation is harmful, but a good immune response and repair are essential for maintaining bodily functions. For people who want to age healthily, it is therefore important to pay attention to inflammatory processes without completely suppressing them.

The insights from this research help to better understand how cellular ageing processes can be influenced without negative consequences for lifespan.

Source: Reason