MYSM1 Overexpression Extends Life in Mice via a Reduced Senescent Cell Burden

Senescent cell accumulation is an important cause of degenerative aging. Senescent cells cease replication and begin to secrete an inflammatory mix of signals that disrupt tissue structure and function. These cells are created constantly, largely as a result of somatic cells hitting the Hayflick limit on cellular replication, but also as a result of injury, molecular damage, inflammation, and the like. Near all senescent cells are rapidly destroyed, either via programmed cell death mechanisms, or via the immune system. This clearance falters with age, however, slowing down, becoming less efficient, and allowing senescent cells to accumulate, disrupt tissue function, and provoke chronic inflammation. The targeted destruction of senescent cells has been shown - in animal models - to reverse the progression of many age-related conditions and extend healthy life span. It is easy to demonstrate such results, and many research groups have used many different methods to destroy senescent cells. To the extent that these errant cells are removed, benefits follow. As these demonstrations have accumulated over the years, researchers have broadened their investigations of the biochemistry of senescent cells. One class of outcome of this work is represented by today's open access paper. Researchers have identified a gene that affects the burden of cellular senescence, and find that adjusting expression levels down or up also adjusts lifespan as well, due to there being great...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs