The association between the increase in life expectancy in humans and age-related changes in the immune system promotes that individuals are exposed longer to endogenous and environment antigens which allows an activation of the innate immune system and the subsequent establishment of a low grade chronic inflammation state with an increased expression of proinflammatory cytokines (tumor necrosis factor alpha, interleukin 6, etc.). This inflammatory state referred as inflammaging is characterized by a inflammatory origin of aging given by the activation of cellular systems responsible of gene promotion and suppression as the nuclear factor kappa B, sirtuins, forkhead box O and KLOTHO, who are directly or indirectly involved in cellular mechanisms of resistance to oxidative stress, apoptosis and nucleic acids transcriptional mistakes repair. The activation of these cellular systems is associated with the pathogenesis of several chronic and degenerative diseases such as Alzheimer's disease, late-onset diabetes or cardiovascular diseases. However, we are placed in a crossroad because we can not establish whether this inflammatory state observed in the aging process is responsible of development of degenerative diseases or if the presences of these chronic diseases are responsible for this inflammatory state of aging. Evidence in centenarians who are healthy and have preserved functional status has shown that there is a chronic inflammatory state present among them but is balanced by a higher expression of anti-inflammatory molecules.
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