Abstract
DNA methylation involves the covalent transfer of a methyl group to the C-5 position of the cytosine ring on a DNA strand. DNA methylation is both heritable and modifiable and can affect gene expression. In recent years, epigenome-wide association studies using high-throughput technologies have associated variation in DNA methylation levels with normal and pathological aging processes in human populations. DNA methylation patterns have been used to construct epigenetic clocks which can serve as potential biomarkers of age-related diseases. Age acceleration, as determined using these epigenetic clocks, has been strongly linked to common diseases including cancer, neurodegenerative diseases, metabolic diseases, and cardiovascular diseases. Identification of these robust associations between DNA methylation and aging may provide new potential therapeutic avenues for preventing and treating age-related diseases. This review focuses on the role of DNA methylation in aging processes and recent advances in epigenome-wide association studies (EWASs) reporting associations between DNA methylation and age-related diseases.
Highlights
The definition of epigenetics has been modified over decades
Epigenetic modifications may alter the accessibility to DNA and chromatin
There are studies suggesting that small-interfering RNA target TATA-box sequences, blocking the initiation of transcription without modifying histones or DNA [6]
Summary
The definition of epigenetics has been modified over decades. In the mid-twentieth century, epigenetics was defined as the development of a complex organism from a zygote and all processes within [1, 2]. Epigenetic modifications may alter the accessibility to DNA and chromatin These may involve the recruitment or exclusion of various factors that regulate gene transcription. DNA methylation provided an explanation for the heritability of gene expression through somatic cell divisions [5] Another epigenetic mechanism contributing to the regulation of gene expression involves histone variants and modifications, which alter the chromatin structure and subsequent access of transcription machinery. There are studies suggesting that small-interfering RNA (siRNA) target TATA-box sequences, blocking the initiation of transcription without modifying histones or DNA [6]. Together, these mechanisms demonstrate the complex cooperation of different epigenetic mechanisms for the regulation of gene expression
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