Chronic inflammation is an important aspect of aging, a process that stems from low-level biochemical damage and cellular dysfunction, and that then contributes to the progression of age-related disease and tissue dysfunction.
Chronic inflammation sustained over years accelerates all of the common fatal age-related conditions: it disrupts tissue maintenance, and leads to fibrosis, immune dysfunction, and many more issues. The chronic inflammation of aging is important enough that beneficial therapies have been built on the basis of suppressing inflammation directly, without addressing its causes. Treatments that actually address the causes should be very much better at the end of the day, of course.
Interventions that have been demonstrated to slow aging in laboratory species tend to act to suppress the age-related increase in inflammation – they would have to, in order to achieve the outcome of a longer, healthier life in these animals. Calorie restriction is the best studied of these interventions, and a wide range of calorie restriction mimetic drugs have arisen from this field of research, compounds that mimic a fraction of the overall metabolic response to a lower intake of calories. Today's open access paper reviews what is known of the way in which mechanisms of the calorie restriction response act to reduce chronic inflammation and its impact on age-related disease.
A sizable fraction of the inflammation of aging arises from the presence of senescent cells. These cells grow in number with age, and their signaling produces a range of detrimental effects on surrounding tissue, of which chronic inflammation is just one – though, as noted here, an important one. Calorie restriction adopted in later life doesn't impact the burden of cellular senescence to anywhere near as great a degree as the use of senolytic drugs can achieve by selectively destroying senescent cells. That point is worth keeping in mind while looking over the paper noted here.
Source: Fight Aging!