Scientists Discover A Molecular Switch That Can Reverse Chronic Inflammation And Aging

Chronic inflammation is the leading cause of stress, age-related diseases, including diabetes, heart diseases, autoimmune conditions, and several other devastating diseases including Alzheimer’s, Parkinson’s and cancer.

Experts at the University of California, Berkeley have identified a molecular switch that can control the immune machinery that is responsible for chronic inflammation.

“My lab is very interested in understanding the reversibility of aging,” Berkeley News quoted the study’s senior author Danica Chen, associate professor of metabolic biology, nutritional sciences and toxicology at UC Berkeley. “In the past, we showed that aged stem cells can be rejuvenated. Now, we are asking: to what extent can age be reversed? And we are doing that by looking at physiological conditions, like inflammation and insulin resistance, that have been associated with aging-related degeneration and diseases.”

Previous studies have pointed out that the rate of aging can be slowed. But, there has been no clarity pertaining to the extent to which aging-related conditions can be reversed.

The researchers developed a cell-based system that models aging-associated inflammation and insulin resistance in metabolic tissues during the aging process.

They were able to demonstrate that deacetylating or switching off a protein called ‘SIRT2’ not only prevented but can be targeted to reverse aging-related inflammation as well as insulin resistance. SIRT2 is an immune protein that is responsible for sensing potential threats to the body and causing an inflammatory response.

The mechanism: the acetylation can be a switch. When the protein SIRT2 is acetylated, the inflammasome, which is the protein complex responsible for inflammation, gets switched on. Therefore, deacetylating it switches off the inflammasome and reverses inflammation.

The protein SIRT2 is responsible for deacetylating the NLRP3 inflammasome. Among mice that were bred with a genetic mutation that prevented SIRT2 production exhibited more signs of inflammation, aging and insulin resistance. They also found that mice who were injected with deacetylated or switched off version of the inflammasome had improved insulin resistance.

The findings of the study have vital implications in treating major human chronic diseases. Also, understanding the reversibility of aging-related conditions and using it to aid a drug development can make a huge difference in treating several debilitating aging-related diseases.