[Prospects for the search for peptides for specific regulation of aging.]

We propose a hypothesis that the causes of aging are not random events, but regular processes due to the dysfunction of species-specific transposons. The hypothesis is justified by the fact that the average life expectancy differs significantly between species. In addition, genomes of different species differ in the composition and arrangement of transposons in them, which control the differentiation of cells in different tissues and at different stages of development. We presented literature data confirming this assumption and substantiating the key role of transposons in regulating gene expression in ontogenesis. In the terminally differentiated cells, the mechanisms of the silencing of mobile elements are activated, which are depleted, which leads to the dysfunction of gene-regulated regulatory networks controlled by transposons, the aging and development of age-associated pathology. Mobile elements are capable of transposing into strictly defined genomic loci, transcribed into functional RNAs that are translated into peptides. We propose that the detection of changes in the activity of specific mobile elements associated with aging through the analysis of non-coding RNA of transposon origin can be the basis for developing ways to increase life expectancy and targeted therapy for age-related pathologies, including malignant tumors. A promising direction in this respect may be the study of peptides that affect the expression of specific transposons and non-coding RNAs.