Molecular switches reverse chronic inflammation and aging, Chronic inflammation that occurs when age, stress, or environmental toxins hold the immune system in the form of over-prosthesis can cause a variety of devastating diseases, from Alzheimer’s and Parkinson’s to diabetes and cancer.

Scientists at the University of California at Berkeley have now identified a molecular “switch” that controls the immune system responsible for chronic inflammation in the body.

This finding, which was published online on Cell Metabolism on February 6, could lead to new ways to stop or even reverse many of these age-related conditions. Molecular switches reverse chronic inflammation and aging.

“My laboratory is very interested in understanding the reversibility of aging,” said senior author Danika Chen, assistant professor of metabolic biology, nutrition science, and toxicology at UC Berkeley. “In the past, we have shown that old stem cells can be rejuvenated.

Now we ask ourselves: to what extent can aging be reversed? To do this, we examine physiological conditions such as inflammation and insulin resistance, which are associated with degeneration and age-related diseases. ”

In the study, Chen and his team showed that a large collection of immune proteins, known as the NLRP3 inflammation system, which recognizes potential threats to the body and triggers an inflammatory response, are essentially removed by eliminating small amounts of molecular substances in cells. can be a process called deacetylation.

Excessive activation of NLRP3 is associated with a variety of chronic diseases, including multiple sclerosis, cancer, diabetes, and dementia.

Chen’s results show that drugs that target deacetylation or exclusion can help this inflammatory NLRP3 to prevent or treat this condition and the possibility of overall age-related degeneration. Molecular switches reverse chronic inflammation and aging.

“This acetylation can act as a switch,” Chen said. “When acetylation, the inflammatory light turns on. When deacetylation, the inflammatory condition is turned off.”

The team examined macrophages called mice and immune cells and found that a protein called SIRT2 was responsible for the deacetylation of inflammatory NLRP3. Mice bred with genetic mutations that prevent SIRT2 production show more signs of inflammation than their normal counterparts when they are two years old.

These mice also have higher insulin resistance, type 2 diabetes, and metabolic syndrome.

The team also examined older mice whose immune system was destroyed by radiation and then dissolved with blood stem cells that produce a deacetylated version of inflammatory NLLP3 or an acetate version.

Those who were given a deacetylation or “excluded” version of the inflammatory condition increased their insulin resistance after six weeks, showing that shutting down the immune system could actually reverse the course of metabolic disorders.

I think this finding has very important implications for the treatment of serious chronic human diseases, “Chen said. This is also a topical problem because many promising tests for Alzheimer’s disease failed last year. One possible explanation is that treatment also started late and reach the point where there is no turning back.

For this reason, I think it’s more important than ever to understand the reversibility of age-related diseases and use this knowledge to develop drugs for age-related diseases.