[Aging and interrelation of telomeres with transposable elements.]

Telomere dysfunction and changes in their length during aging of an organism is a reflection of more global processes in the genome, which are caused by the regulatory influence of transposable elements sequentially activated during ontogenesis. This consequence is due to the fact that centromeres and centromeric proteins, telomeres and telomerases, introns and spliceosome components, transcription factors and their binding sites, noncoding RNAs and their targets in protein coding gene sequences have evolved from transposable elements. The relationship of these structural-functional elements of the genome dynamically changes in individual development and depends on the characteristics of successive activations and transpositions of the transposable elements. Each species is characterized by a specific set of transposable elements and associated tandem repeats, which affects the epigenetic regulation of ontogenesis. These tandem repeats are mainly contained in centromeres and telomeres, the specific influence of researchers on which is promising for developing ways of regulating life expectancy. This is due to the ability of ribozymes and peptides to interact with specific DNA nucleotide sequences, especially as part of tandem repeats. An important approach to the study of the relationship of transposons with telomeres, centromeres and subtelomeric regions for the regulation of aging can be the study of the role of their uniting peptides and miRNA, whose complex application has a high potential of geroprotective efficiency.