TY - JOUR
T1 - Genomic instabilities, cellular senescence, and aging
T2 - In vitro, in vivo and aging-like human syndromes
AU - Lidzbarsky, Gabriel
AU - Gutman, Danielle
AU - Shekhidem, Huda Adwan
AU - Sharvit, Lital
AU - Atzmon, Gil
N1 - Publisher Copyright: ©2018 Lidzbarsky, Gutman, Shekhidem, Sharvit and Atzmon.
PY - 2018/4/1
Y1 - 2018/4/1
N2 - As average life span and elderly people prevalence in the western world population is gradually increasing, the incidence of age-related diseases such as cancer, heart diseases, diabetes, and dementia is increasing, bearing social and economic consequences worldwide. Understanding the molecular basis of aging-related processes can help extend the organism's health span, i.e., the life period in which the organism is free of chronic diseases or decrease in basic body functions. During the last few decades, immense progress was made in the understanding of major components of aging and healthy aging biology, including genomic instability, telomere attrition, epigenetic changes, proteostasis, nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and intracellular communications. This progress has been made by three spear-headed strategies: in vitro (cell and tissue culture from various sources), in vivo (includes diverse model and non-model organisms), both can be manipulated and translated to human biology, and the study of aging-like human syndromes and human populations. Herein, we will focus on current repository of genomic "senescence" stage of aging, which includes health decline, structural changes of the genome, faulty DNA damage response and DNA damage, telomere shortening, and epigenetic alterations. Although aging is a complex process, many of the "hallmarks" of aging are directly related to DNA structure and function. This review will illustrate the variety of these studies, done in in vitro, in vivo and human levels, and highlight the unique potential and contribution of each research level and eventually the link between them.
AB - As average life span and elderly people prevalence in the western world population is gradually increasing, the incidence of age-related diseases such as cancer, heart diseases, diabetes, and dementia is increasing, bearing social and economic consequences worldwide. Understanding the molecular basis of aging-related processes can help extend the organism's health span, i.e., the life period in which the organism is free of chronic diseases or decrease in basic body functions. During the last few decades, immense progress was made in the understanding of major components of aging and healthy aging biology, including genomic instability, telomere attrition, epigenetic changes, proteostasis, nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and intracellular communications. This progress has been made by three spear-headed strategies: in vitro (cell and tissue culture from various sources), in vivo (includes diverse model and non-model organisms), both can be manipulated and translated to human biology, and the study of aging-like human syndromes and human populations. Herein, we will focus on current repository of genomic "senescence" stage of aging, which includes health decline, structural changes of the genome, faulty DNA damage response and DNA damage, telomere shortening, and epigenetic alterations. Although aging is a complex process, many of the "hallmarks" of aging are directly related to DNA structure and function. This review will illustrate the variety of these studies, done in in vitro, in vivo and human levels, and highlight the unique potential and contribution of each research level and eventually the link between them.
KW - Aging
KW - Cellular senescence
KW - DNA damage
KW - Epigenetics
KW - Telomeres
UR - http://www.scopus.com/inward/record.url?scp=85050110472&partnerID=8YFLogxK
U2 - https://doi.org/10.3389/fmed.2018.00104/full
DO - https://doi.org/10.3389/fmed.2018.00104/full
M3 - Review article
SN - 2296-858X
VL - 5
JO - Frontiers in Medicine
JF - Frontiers in Medicine
IS - APR
M1 - 104
ER -