The Inflammasome as a Target for the Next Generation of Anti-Inflammatory Therapies

With advancing age, a wide range of mechanisms act to provoke the immune system into a state of constant inflammatory signaling and activation. Age-related mitochondrial dysfunction leads to mislocalized mitochondrial DNA fragments that trigger the cGAS-STING pathway to provoke inflammation. Senescent cells produce pro-inflammatory signaling, and their numbers increase with age. Visceral fat tissue produces signaling similar that resulting from infected cells. The increased presence of protein aggregates aggravates immune cells inside and outside of the brain. And so forth. Given all of this, actually fixing the issue of age-related chronic inflammation will likely require control over a great deal of the underlying biochemistry of aging itself. Nonetheless, chronic inflammation is clearly a major problem that produces sizable downstream issues. It is highly disruptive to tissue function, accelerating all of the major fatal age-related conditions. If there are shortcuts to suppress excessive, chronic inflammation without affecting the necessary short-term inflammation required for the immune system to function, then pursing these shortcuts may turn out to be at least as beneficial as, say, control over raised blood pressure. Unfortunately, most of the approaches developed to date do poorly when it comes to avoiding suppression of necessary immune function. As discussed in today's open access paper, there is the hope that targeting the immune sensors called infla...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs