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Gene & Protein in Disease Buccal mucosa and aging

Table 3. Examples of biomolecular changes in aging
Type Effect Examples References
Pathways Mediated cell survival, growth, and AKT1, ATM, FOXO1, FOXO3, GHR, HIF1A, IGF1, 96
DNA repair IGF1R, PIK3CA, and PIK3CB
Mediated apoptosis/senescence BAX, BCL2, CDK4, CDK6, CDKN1A (P21), CDKN2A 96
signaling pathway (P16), CDKN2B (P15), FAS, and TP53
Autophagy/Survival AMPK subunits (PRKAA1, PRKAA2, PRKAB2, 96
PRKAG1, PRKAG2), SIRT1, RPS6KB1 (S6K), and TSC2
Cross-talk between the aging KL, MYC, NFKB1, NFKB2, PPARGC1A, PTEN, TGFB1, 96
pathways and TGFBR2
Sirtuins are involved in metabolic Sir2, SIRT1, PGC-1α, Ku70, NF-κB, AceCS1, MEF2 and 127
control, apoptosis, cell survival, p53, FOXO transcription factors
development, inflammation, and
healthy aging
Lifespan regulation through PGC-1α, PGC-1β, NRF-1, and ERRα 127
mitochondrial DNA
Stable housekeeping genes in aging 18s, HPRT1, ACTB, and TMEM199 128,129
Epigenetics DNA methylation, histone 130
modifications, non-coding RNAs
Natural killer cells in the Biomarkers modifications during IFN-γ, TNF-α, TNF-β, GM-CSF, CXCR3, CCR6, CCR9, 69,70,117,131-137
dim
buccal mucosa (CD56 cells aging CCR4, IL-10, IL-4, IL6, IL-13, IL-2, IL-15, and IL-12
and CD56 bright cells)
Abbreviations: IFN-γ: Interferon-γ; TNF-α: Tumor necrosis factor-α; TNF-β: Tumor necrosis factor-β; IL: Interleukin.

cells and the aging process can be regulated through invasive methods and identifying molecular biomarkers
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epigenetic changes in the body. to monitor cellular damage caused by both external
Epigenetics, including DNA methylation, histone and internal factors. Environmental hazards are well-
modifications, and non-coding RNAs, plays a crucial role documented contributors to aging, leading to DNA
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in the regulation of aging. These epigenetic modifications damage and premature aging, which, in turn, increase
are key regulators of gene expression and influence the incidence of diseases and premature mortality. As a
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cellular responses to environmental exposures, as well as result, molecular biomarkers are being investigated for
99
changes associated with aging. Various environmental their potential to assess DNA damage in cells, including
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factors, such as diet, exposure to toxins, stress, smoking, buccal and NK cells found in the oral mucosa, to enable the
and childhood trauma, can significantly impact individual screening and diagnosis of individuals at risk of premature
epigenetic clocks and gene regulation. These changes aging. This review aims to clarify the intricate relationship
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are directly linked to longevity across a wide range of between environmental hazards, cellular senescence,
organisms, from yeast to humans. 124 and DNA damage, thereby aiding in the development of
diagnostic and preventive measures. Further research
Exposure to environmental chemicals can lead
to changes in epigenetic biomarkers and genome is essential to fully understand the role of biomarkers in
function, 125,126 which accelerate aging by influencing assessing DNA damage during aging and to identify new
targets for strategies aimed at preventing and treating
caloric restriction, mitochondrial function, the activity
of housekeeping genes, and metabolic enzyme control. premature aging and age-related health issues.
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Figure 4 illustrates how these factors contribute to cellular Acknowledgments
senescence. Despite these findings, further efforts are
needed to identify the genetic and epigenetic factors that The authors would like to acknowledge Dr. Johannes
contribute to aging and to determine their precise effects, Martin Schmid from the Department of Respiratory
thereby expanding the list of contributing factors (Table 3). Diseases and Allergy, Aarhus University Hospital, for his
support in editing the English of this paper.
7. Conclusion
Funding
Given the profound impact of aging on mortality and disease
susceptibility, researchers are continually developing non- None.

Volume 3 Issue 4 (2024) 7 doi: 10.36922/gpd.4418