CHRONIC INFLAMMATION IN THE ELDERLY: MECHANISMS AND ASSOCIATION WITH ATHEROSCLEROSIS

In 2000 Claudio Franceschi first used the term “inflammageing” derived from the English words “inflammation” and “age”. This term refers to the development of chronic inflammation in the elderly, which is characterized by a high level of pro-inflammatory markers of cells and tissues. Cellular aging can be triggered by a variety of factors: critical telomere shortening, permanent DNA damage, epigenetic damage, mitochondrial dysfunction, and an increase in the number of molecular fragments associated with cell damage.
A large number of markers have been found to reveal the pro-inflammatory status, such as interleukin (IL) 1, IL-1ra (IL-1 receptor antagonist protein), IL-6, -8, -13, -18, C-reactive protein, interferons α, β, transforming growth factor β, tumor necrosis factor α and its soluble receptors and SAA-1 (serum amyloid А1). The molecular mechanisms associated with aging and age-related diseases are not clear yet, while sluggish chronic inflammation is one of the leading mechanisms for the atherosclerosis development. Remodeling of the immune system with the increasing production of pro-inflammatory cytokines and NLRP3 inflammasomes also play a key role in the maintenance of chronic inflammation due to its ability to pick up a variety of age-related dangerous signals that trigger the immune response and subsequent inflammation and may act as a factor of the atherosclerosis development.
Thus, pro-inflammatory factors of the immune system play an important role in pathogenesis of atherosclerosis,
especially at an early stage, involving various mechanisms of action that boost atherosclerotic changes.