Accepted_test

Research of non-monotonic aging changes based on multiomics data
by Anastasija Gorbarenko | Gleb Bobkov | Aleksey Alekseev | Bioinformatics Institute, Kantemirovskaya st. 2A, 197342, St. Petersburg, Russia | ITMO, Kronverksky pr., 49 A, 197101, St. Petersburg, Russia | Lomonosov Moscow State University
Abstract ID: 764
Event: BGRS-abstracts
Sections: Section “Genetics and systems biology of aging”

At the age around 37, various molecular alterations occur in human organisms, including dysregulated gene expression, altered metabolite levels, somatic mutations, epimutations, and accumulated molecular damage [7 - 10]. Age transition in 23±2 years old (y.o.) is also very important for the system biology of aging: first increasing of MDA (malondialdehyde, marker of oxidative stress) occurs at this age [12]. Significant stages in the aging process also occur around ages 24 and 60, where molecular and physiological changes become most pronounced [11 - 13]. Wide known “hallmarks of aging” involve genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulation of nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. These mechanisms contribute to aging at molecular, cellular, and systemic levels [6, 14, 15], but interaction between cellular and systemic aging is still unclear. This study aims to obtain the most relevant cellular aspect, associated with metabolic transition of aging around 37 through multiomics analysis, including epigenomics and RNA-sequencing data.