Epigenetic biomarkers in aging and longevity: Current and future application

The aging process has been one of the most necessary research fields in the current century, and knowing different theories of aging and the role of different genetic, epigenetic, molecular, and environmental modulating factors in increasing the knowledge of aging mechanisms and developing appropriate diagnostic, therapeutic, and preventive ways would be helpful. One of the most conserved signs of aging is epigenetic changes, including DNA methylation, histone modifications, chromatin remodeling, noncoding RNAs, and extracellular RNAs. Numerous biological processes and hallmarks are vital in aging development, but epigenomic alterations are especially notable because of their importance in gene regulation and cellular identity. The mounting evidence points to a possible interaction between age-related epigenomic alterations and other aging hallmarks, like genome instability. To extend a healthy lifespan and possibly reverse some facets of aging and aging-related diseases, it will be crucial to comprehend global and locus-specific epigenomic modifications and recognize corresponding regulators of health and longevity. In the current study, we will aim to discuss the role of epigenomic mechanisms in aging and the most recent developments in epigenetic diagnostic biomarkers, which have the potential to focus efforts on reversing the destructive signs of aging and extending the lifespan. Different patterns of epigenetic alterations. The various factors that play a key role in DNA methylation, histone modifications, chromatin remodeling, and non-coding RNA (miRNA) are shown to be altered during aging. Upregulation or downregulation of these factors over time elicit different changing patterns at the epigenomic level, so-called “Epigenetic alterations”. A summary of these epigenetic modifications during aging has been indicated. Epigenetic changes are in close interaction with other hallmarks of aging, and epigenomic instability causes mitochondrial dysfunction, loss of proteostasis, dysbiosis, genomic instability, loss of chromatin, cellular senescence, disabled autophagy, deregulated nutrient sensing, telomere erosion, inflammation, stem cell exhaustion, and altered cellular communication, which results in aging. DNMT, DNA methyl transferase; MBD, methyl-CpG-binding domain; HAT, Histone acetyltransferase; HMT, Histone methyl transferase; HDAC, histone deacetylase; miRNA, micro-RNA; HP1α, heterochromatin protein 1α; NuRD, nucleosome remodeling and histone deace