ANGPTL2 Knockout Reduces Inflammation and Slows Muscle Loss in Mice

The gene ANGPTL2 is starting to look like an interesting basis for therapy, something to bump closer to the top of the lengthy list of targets to consider for first generation human gene therapies. In animal studies, lowering the level of protein produced by this gene has been shown to reduce chronic inflammation in older individuals and slow progression towards heart failure. These effects might be mediated through the presence of senescent cells in the cardiovascular system, in that it is these cells that are the primary producers of ANGPTL2. One of the most easily measured consequences of the growing numbers of senescent cells in older tissues is a higher level of inflammation. Here researchers show that loss of ANGPTL2 can slow the age-related decline in muscle mass that takes place in later life, a condition known as sarcopenia. They also consider cellular senescence to be a plausible mediating mechanism for the detrimental effects of ANGPTL2 when it is present, and certainly there is plenty of evidence to link sarcopenia with chronic inflammation. Raised levels of inflammation and other activities of senescent cells derail the normal processes of tissue maintenance. If this is the case, and ANGPTL2 does cause harm due to increased levels of cellular senescence or increased activity of senescent cells, then senolytic therapies that destroy senescent cells should capture all of the benefits of reduced levels of ANGPTL2, rendering gene therapy approaches redundant i...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs