Abstract
Proper functioning of cells—their ability to divide, differentiate, and regenerate—is dictated by genomic stability. The main factors contributing to this stability are the telomeric ends that cap chromosomes. Telomere biology and telomerase activity have been of interest to scientists in various medical science fields for years, including the study of both cancer and of senescence and aging. All these processes are accompanied by telomere-length modulation. Maintaining the key levels of telomerase component (hTERT) expression and telomerase activity that provide optimal telomere length as well as some nontelomeric functions represents a promising step in advanced anti-aging strategies, especially in dermocosmetics. Some known naturally derived compounds contribute significantly to telomere and telomerase metabolism. However, before they can be safely used, it is necessary to assess their mechanisms of action and potential side effects. This paper focuses on the metabolic potential of natural compounds to modulate telomerase and telomere biology and thus prevent senescence and skin aging.
Highlights
This is supported by the observation that telomeres in cancer cells are significantly shorter than in normal cells, which results from the fact that carcinogenesis is preceded by intensive replication, followed by the crisis and, restoration of human telomerase reverse transcriptase (hTERT) expression [130]
The answers to the questions of how the aging process is initiated, what its stages are, and their consequences will enable the design of strategies that can slow down these processes
The noncanonical functions of the critical telomerase subunit are associated with antioxidant activity
Summary
These structures are composed of (a) specific DNA repeat sequences of 50 TTAGGGn (conserved in vertebrates), and (b) the shelterin complex, which consists of six proteins that maintain the structure and control telomere metabolism [1] Their primary function is to protect the linear chromosome ends against damage which could lead to DNA breaks such as single-strand breaks (SSB) or double-strand breaks (DSB). Many theories suggest that various aging phenotypes appear because of the age-dependent accumulation of damage [6,7] This may eventually lead to senescence, which is defined as irreversible cell-cycle arrest driven by a variety of mechanisms, including telomere shortening, genotoxic stress, mitogens, inflammatory cytokines, and activation of the p53 tumor suppressor and/or the cyclin-dependent kinase inhibitor p16 [8]. Skin cells’ (and most somatic cells’) proliferative potential and resistance to apoptosis are decreased, and the secretion of factors that promote inflammation and tissue decline increases [10,11,12]
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