Aging
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Review|Volume 1, Issue 2|pp 182—190

Chromatin modifications: The driving force of senescence and aging?

Teresa DiMauro1, Gregory David1,2
  • 1Department of Pharmacology, NYU Langone Medical Center, New York, NY 10016, USA
  • 2NYU Cancer Institute, NYU Langone Medical Center, New York, NY 10016, USA
Received: January 20, 2009Accepted: February 11, 2009Published: February 13, 2009

Copyright: © 2009 DiMauro et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

An emerging field of investigation in the search for treatment of human disease is the modulation of chromatin modifications. Chromatin modifications impart virtually all processes occurring in the mammalian nucleus, from regulation of transcription to genomic stability and nuclear high order organization. It has been well recognized that, as the mammalian cell ages, its chromatin structure evolves, both at a global level and at specific loci. While these observations are mostly correlative, recent technical developments allowing loss-of-function experiments and genome-wide approaches have permitted the identification of a causal relationship between specific changes in chromatin structure and the aging phenotype. Here we review the evidence pointing to the modulation of chromatin structure as a potential driving force of cellular aging in mammals.