Autophagy is an important biological mechanism to maintain homeostasis in all animal tissues. Many studies have attempted to reveal the relationship between decreased autophagy levels and aging in animals, but there is still no clear answer.
A team led by professor Carmela Abraham of Boston university school of medicine found that Rubicon, a protein factor, inhibits autophagy by controlling a step in the autophagy process. Expression levels of Rubicon protein in the tissues of worms, flies and mice were found to increase in an age-related manner. Autophagy helps break down damaged organelles while avoiding a host of stress-related diseases, including cancer, neurodegenerative diseases and metabolic syndrome. Recent studies have found that decreased autophagy levels are associated with the aging process in animals. Although there are other ways to slow down the aging process by increasing autophagy levels in aging animals, no research has pinpointed the reasons for the decline.
Professor Carmela Abraham said: "we have known that Rubicon protein is associated with inhibition of autophagy, and knocking out Rubicon protein in mice can eliminate autophagy-related liver diseases, so we suspected that Rubicon protein may directly affect aging through its interaction with autophagy."
In this study, the researchers found elevated levels of Rubicon protein in a variety of aging organisms. When inhibiting the expression of Rubicon protein, all model animals exhibited higher autophagy levels, which improved many senescence related factors and extended the life span of model organisms.
The study suggests that increased levels of Rubicon protein, which may be key to extending healthy life in humans, lead to decreased autophagy in aging animals.