Abstract
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.
Highlights
The chronological age, the number of years since birth, does not necessarily correspond to the same age-linked average physical characteristics reflected in biological functionality of the organs, tissues, and cells [1]
Multiple factors are involved in regulation of physical aging [3], in this article, we have focused on molecular biology of senescence and current advances in the clinical science of aging
The study of the mechanisms of regulation of sphingolipid catabolism demonstrated that the TP53-dependent DNA damage response regulates the function of neutral sphingomyelinase 2 at the mRNA level by TP53 in the context of the DNA damage response, which is associated by epigenetic mechanisms, a combination of DNA methylation and histone deacetylation, induced by all-trans retinoic acid (ATRA) [75]
Summary
The chronological age, the number of years since birth, does not necessarily correspond to the same age-linked average physical characteristics reflected in biological functionality of the organs, tissues, and cells [1]. The age-associated physiology is defined by intrinsic and extrinsic interactions with stress during individual development and growth. Intrinsic aging-related factors and phenotypes are associated with the genetic material and genetic predisposition inherited from parents [2]. The age of the genome can be evaluated using molecular and biological parameters, including specific age-linked characteristics that indicate age-related changes in DNA, RNA, proteins, and/or metabolites in various tissues and cells. These specific markers of aging in epithelial cells will be discussed below
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