Genetics and Epigenetics of Aging and Longevity 2.0

Dear Colleagues,

It is my pleasure to announce the launch of a new Special Issue on the topic of “Genetics and Epigenetics of Aging and Longevity”.

Lifespan is a complex quantitative characteristic that makes a significant contribution to Darwinian adaptiveness. The disclosure of the genetic and epigenetic structure of longevity is a fundamental problem of the evolution of ontogeny, evolutionary genetics, and molecular gerontology. Under optimal conditions, the lifespan is determined by the aging rate. The aging process is made up of interrelated processes that take place at the organismal, tissue, cellular, molecular, and genetic levels. These include deregulation processes of homeostasis maintenance, metabolic reactions, and sending intra­ and intercellular signals, accumulation of senescent cells, damaged organelles and macromolecules, epigenetic changes, and genetic instability. The objective of this topic is to summarize the available information about underlying genetic and epigenetic determinants of longevity and aging. Genes and signaling pathways that regulate stress response, metabolism, growth of cells and organisms, maintaining of genome and proteome integrity, mitochondria quality, inflammatory response, apoptosis and selection of viable cells, as well as circadian rhythms are involved in longevity. The redistribution of energy resources from one pathway to the other can induce or inhibit the “longevity program”, providing increased vitality and aging slowdown. Based on the analysis of geroprotective potential of examined genes’ regulation, the main targets have been identified to slowdown aging and achieve healthy longevity. These trends include heterochromatin recovery, retrotransposition suppression, and aneuploidy elimination; restoring the acidity of lysosomes; telomere elongation; suppression of chronic inflammation; elimination of protein crosslinks; elimination of senescent cells; recovery of NAD+ levels; inhibition of mTOR, S6K, TGF­β, and AT1; and controlled activation of the “longevity program” genes FOXO, AMPK, PGC1α, and NRF2. This topic could help toward a better understanding of the mechanisms of aging and longevity and identification of new biomarkers of aging and longevity interventions and could increase their translational potential.

Prof. Alexey Moskalev
Guest Editor

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