Aging puzzle: A closer look on the complex dilemma of autologous stem cell therapy

Figure 4 The cellular consequences of telomere shortening through three distinct pathways: Telomere inhibition, sub-telomere amplification, and telomere recombination. In telomere inhibition, progressive shortening triggers DNA damage responses and genomic instability, leading to chronological and replicative aging. Sub-telomere amplification may transiently lengthen telomeres but induces replication stress and genomic instability, ultimately resulting in renewed telomere shortening and replicative senescence. Telomere recombination also promotes telomere lengthening; however, it causes DNA replication errors and genomic instability, leading to non-telomeric damage, replicative senescence, and aging.