Special Issue "The Epigenetics of Aging and Longevity"
A special issue of Genes (ISSN 2073-4425).
Deadline for manuscript submissions: 31 October 2017
Special Issue Editors
Prof. Dr. Jessica Tyler
Weill Cornell Medicine, Department of Pathology and Laboratory Medicine, New York, NY, USA
Chromatin assembly, histone modifications, chromatin remodeling, DNA double strand break repair, replicative aging
Dr. Jay E. Johnson
Orentreich Foundation for the Advancement of Science, Cold Spring, NY, USA
methionine restriction, chronological lifespan, Saccharomyces cerevisiae, budding yeast, aging, healthspan, longevity, senescence, autophagy
Special Issue Information
A growing body of evidence demonstrates that both genetic and epigenetic alterations contribute to aging. In contrast to genetic changes, the reversible nature of epigenetic mechanisms makes these pathways promising avenues for the development of regimens against age-related decline and disease.
With the advent of techniques for genome-wide analysis of histone modifications and DNA methylation, we are now learning that aging is accompanied by a wealth of changes to the epigenetic information. These age-associated changes in the epigenetic information alter the chromatin structure over time, in turn causing transcriptional changes, genomic instability and activation of transposons that drive the aging process. Furthermore, small molecules are being utilized to alter the epigenetic information in order to counter the aging process in model organisms. The best-characterized pathway connecting the environment to the epigenome is nutrient signaling. Exciting progress is being made in understanding how nutrients influence aging and how nutrients, including altered diets, can be utilized to promote longevity.
In this Special Issue, we would like to invite submissions of original research or review articles on topics relevant to “the epigenetics of aging and longevity”. We hope to gather together knowledge to empower efforts towards the effective and safe extension of lifespan and health span in humans. We look forward to receiving your contributions.
Prof. Dr. Jessica Tyler
Dr. Jay E. Johnson
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Genes is an international peer-reviewed open access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
replicative lifespan, chronological lifespan, longevity, aging, health span, dietary restriction, methionine restriction, autophagy, epigenome, epigenetics
This special issue is now open for submission, see below for planned papers
The below list represents only planned manuscripts. Some of these
manuscripts have not been received by the Editorial Office yet. Papers
submitted to MDPI journals are subject to peer-review.
Tentative Title: MicroRNA-29: a miR for rusty aging
Authors: Sfera A.; Osorio C.; Price A.; Anger J.; Cummings M.
Abstract: Excess iron induces cellular senescence in various body tissues, likely triggering organismal aging via hydroxyl radicals, including reactive oxygen species (ROS). A dysfunctional iron homeostasis was associated with pathology ranging from tumorigenesis to metabolic syndrome and Alzheimer’s disease. Iron deprivation as an intervention for restoring iron homeostasis is a well-established cancer treatment which was also found beneficial in metabolic dysfunction and neurodegenerative disorders.
The body responds to iron overload by activating the tumor suppressor genes, including protein 53 (p53) which is up-regulated by microRNA-29 (miR-29) and disabled by forkhead box protein O4 (FOXO4). Blocking FOXO4 deacetylation, may enable miR-29-p53 complex to initiate natural senolysis.
In this review article, we take a closer look at what is currently known about the relationship between iron-induced tumorigenesis, cellular senescence, dysmetabolism and neurodegeneration, with special emphasis on dietary interventions, the microbiome and iron absorption.
Tentative Title: Histone macroH2A1: a chromatin point of intersection between fasting, senescence and cellular regeneration
Authors: Lo Re, O; Vinciguerra, M.
Abstract: Histone variants confer chromatin unique properties. They have specific genomic distribution, regulated by specific deposition and removal machineries. Histone variants, mostly of canonical histones H2A, H2B and H3, have important roles in early embryonic development, in lineage commitment of stem cells, in the converse process of somatic cell reprogramming to pluripotency and, in some cases, in the modulation of animal aging and life span. MacroH2A1 is a variant of histone H2A, present in two alternatively exon-spliced isoforms macroH2A1.1 and macroH2A1.2, regulating cell plasticity and proliferation, during pluripotency and tumorigenesis. Furthermore, macroH2A1 participates in the formation of senescence-associated heterochromatic foci (SAHF) in senescent cells, and multiple lines of evidence in genetically modified mice suggest that macroH2A1 integrates nutritional cues from the extracellular environment to transcriptional programs. Here, we review current molecular evidence based on next generation sequencing data, cell assays and in vivo models supporting different mechanisms that could mediate the function of macroH2A1 in health span and life span. We will further discuss context-dependent and isoform-specific functions. The aim of this review is to provide guidance to assess histone variant macroH2A1 potential as therapeutic intervention point.