Epithelial Cell Transformation and Senescence as Indicators of Genome Aging: Current Advances and Unanswered Questions

The recent advances in deciphering the human genome allow us to understand and evaluate the mechanisms of human genome age-associated transformations, which are largely unclear. Genome sequencing techniques assure comprehensive mapping of human genetics; however, understanding of gene functional interactions, specifically of time/age-dependent modifications, remain challenging. The age of the genome is defined by the sum of individual (inherited) and acquired genomic traits, based on internal and external factors that impact ontogenesis from the moment of egg fertilization and embryonic development. The biological part of genomic age opens a new perspective for intervention. The discovery of single cell-based mechanisms for genetic change indicates the possibility of influencing aging and associated disease burden, as well as metabolism. Cell populations with transformed genetic background were shown to serve as the origin of common diseases during extended life expectancy (superaging). Consequently, age-related cell transformation leads to cancer and cell degeneration (senescence). This article aims to describe current advances in the genomic mechanisms of senescence and its role in the spatiotemporal spread of epithelial clones and cell evolution.

Automated summary

Recent advances in deciphering the human genome have allowed a better understanding of age-associated transformations, including gene functional interactions and the impact of single cell mechanisms on aging and disease. Genomic age is defined by a combination of inherited and acquired genetic traits, influenced by internal and external factors, leading to diseases such as cancer and cell degeneration.