Cell reprogramming and physiological aging
Review of research articles published in 2009 that have made or will make a significant contribution to the study of aging – Part 7.
In recent years, much attention has also been paid to the transformation of differentiated cells into induced pluripotent stem cells (iPSCs) by reprogramming the nucleus using certain factors. It is believed that understanding which factors contribute to the reprogramming process is the key to understanding the process of oncogenesis. At the same time, core reprogramming can be considered as a "rejuvenation process". At the same time, it has been demonstrated that tumor suppressor proteins p53 m p16 INK4a play an important role in limiting the possibilities of reprogramming [50-55]. It has been suggested that p53 protein activation is more important for rodent cells, whereas p16 INK4a activation is the main barrier for human cells [50].
Of particular importance for the field of regenerative medicine, which implies the isolation of their own stem cells in elderly patients, is the effectiveness of reprogramming fibroblasts of older people compared with cells of young people. There is an age-associated decrease in the effectiveness of reprogramming, which can be largely overcome by inactivating the tumor suppressor gene p16 INK4a, whose expression in a number of human and mouse tissues increases significantly with aging [50, 55]. The study of these patterns showed that the degree of age-related increase in the expression of p16 INK4a can be assessed in human peripheral blood samples, and the individual expression level of p16 INK4a is an indicative biomarker of the "molecular age" of a person [56]. The same group of researchers also provided new data concerning the relationship between the "snips" located near the CDKN2a/b locus encoding the genes of tumor suppressor proteins p16 INK4a, p15 INK4b and ARF) and the development of atherosclerosis in humans [57]. CDKN2a/b transcript expression is reduced in individuals with alleles associated with an increased risk of the disease. This fact indicates that the development of atherosclerosis may be the result of abnormal, excessive cell proliferation. These data are confirmed by studies according to which mice with increased expression of the CDKN2a/b locus are characterized by delayed aging and increased life expectancy [58].
Continuation: Genetics of aging.
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