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Hot topics in epigenetic mechanisms of aging: 2011
María Berdasco, Manel Esteller
Aging Cell · 2012 · ▲ 88 citations
Abstract
Aging is a complex process that results in compromised biological functions of the organism and increased susceptibility to disease and death. Although the molecular basis of aging is currently being investigated in many experimental contexts, there is no consensus theory to fully explain the aging process. Epigenetic factors, including DNA methylation, histone modifications, and microRNA expression, may play central roles in controlling changes in gene expression and genomic instability during aging. In this Hot Topic review, we first examine the mechanisms by which these epigenetic factors contribute to aging in diverse eukaryotic species including experimental models of yeasts, worms, and mammals. In a second section, we will emphasize in the mammalian epigenetic alterations and how they may affect human longevity by altering stem cell function and/or somatic cell decline. The field of aging epigenetics is ripe with potential, but is still in its infancy, as new layers of complexity are emerging in the epigenetic network. As an example, we are only beginning to understand the relevance of non-coding genome to organism aging or the existence of an epigenetic memory with transgenerational inheritance. Addressing these topics will be fundamental for exploiting epigenetics phenomena as markers of aging-related diseases or as therapeutic targets.
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- 10.1111/j.1474-9726.2012.00806.x
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- 2026-06-03 MST
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APA
Berdasco, M., & Esteller, M. (2012). Hot topics in epigenetic mechanisms of aging: 2011. <em>Aging Cell</em>. https://doi.org/10.1111/j.1474-9726.2012.00806.x
Vancouver
Berdasco M, Esteller M. Hot topics in epigenetic mechanisms of aging: 2011. Aging Cell. 2012. doi:10.1111/j.1474-9726.2012.00806.x.
BibTeX
@article{mara2012Hottop,
title = {Hot topics in epigenetic mechanisms of aging: 2011},
author = {María Berdasco and Manel Esteller},
journal = {Aging Cell},
year = {2012},
doi = {10.1111/j.1474-9726.2012.00806.x},
}
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