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      Epigenetic Clock: DNA Methylation in Aging

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      Author(s): ,
      Publication date (Electronic):
      Journal: Stem Cells International
      Publisher: Hindawi

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          Abstract

          Aging, which is accompanied by decreased organ function and increased disease incidence, limits human lifespan and has attracted investigators for thousands of years. In recent decades, with the rapid development of biology, scientists have shown that epigenetic modifications, especially DNA methylation, are key regulators involved in this process. Regular fluctuations in global DNA methylation levels have been shown to accurately estimate biological age and disease prognosis. In this review, we discuss recent findings regarding the relationship between variations in DNA methylation level patterns and aging. In addition, we introduce the known mechanisms by which DNA methylation regulators affect aging and related diseases. As more studies uncover the mechanisms by which DNA methylation regulates aging, antiaging interventions and treatments for related diseases may be developed that enable human life extension.

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          An epigenetic biomarker of aging for lifespan and healthspan

          Morgan E Levine, Ake T. Lu, Austin Quach … (2018)
          Identifying reliable biomarkers of aging is a major goal in geroscience. While the first generation of epigenetic biomarkers of aging were developed using chronological age as a surrogate for biological age, we hypothesized that incorporation of composite clinical measures of phenotypic age that capture differences in lifespan and healthspan may identify novel CpGs and facilitate the development of a more powerful epigenetic biomarker of aging. Using an innovative two-step process, we develop a new epigenetic biomarker of aging, DNAm PhenoAge, that strongly outperforms previous measures in regards to predictions for a variety of aging outcomes, including all-cause mortality, cancers, healthspan, physical functioning, and Alzheimer's disease. While this biomarker was developed using data from whole blood, it correlates strongly with age in every tissue and cell tested. Based on an in-depth transcriptional analysis in sorted cells, we find that increased epigenetic, relative to chronological age, is associated with increased activation of pro-inflammatory and interferon pathways, and decreased activation of transcriptional/translational machinery, DNA damage response, and mitochondrial signatures. Overall, this single epigenetic biomarker of aging is able to capture risks for an array of diverse outcomes across multiple tissues and cells, and provide insight into important pathways in aging.
          Article 0 comments Cited 976 times – based on 0 reviews     Review now
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            DNA Methylation in Cancer and Aging.

            Michael Klutstein, Deborah Nejman, Razi Greenfield … (2016)
            DNA methylation is known to be abnormal in all forms of cancer, but it is not really understood how this occurs and what is its role in tumorigenesis. In this review, we take a wide view of this problem by analyzing the strategies involved in setting up normal DNA methylation patterns and understanding how this stable epigenetic mark works to prevent gene activation during development. Aberrant DNA methylation in cancer can be generated either prior to or following cell transformation through mutations. Increasing evidence suggests, however, that most methylation changes are generated in a programmed manner and occur in a subpopulation of tissue cells during normal aging, probably predisposing them for tumorigenesis. It is likely that this methylation contributes to the tumor state by inhibiting the plasticity of cell differentiation processes. Cancer Res; 76(12); 3446-50. ©2016 AACR.
            Article 0 comments Cited 372 times – based on 0 reviews     Review now
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              Biological and chemical approaches to diseases of proteostasis deficiency.

              Evan T. Powers, Richard Morimoto, Andrew Dillin … (2009)
              Many diseases appear to be caused by the misregulation of protein maintenance. Such diseases of protein homeostasis, or "proteostasis," include loss-of-function diseases (cystic fibrosis) and gain-of-toxic-function diseases (Alzheimer's, Parkinson's, and Huntington's disease). Proteostasis is maintained by the proteostasis network, which comprises pathways that control protein synthesis, folding, trafficking, aggregation, disaggregation, and degradation. The decreased ability of the proteostasis network to cope with inherited misfolding-prone proteins, aging, and/or metabolic/environmental stress appears to trigger or exacerbate proteostasis diseases. Herein, we review recent evidence supporting the principle that proteostasis is influenced both by an adjustable proteostasis network capacity and protein folding energetics, which together determine the balance between folding efficiency, misfolding, protein degradation, and aggregation. We review how small molecules can enhance proteostasis by binding to and stabilizing specific proteins (pharmacologic chaperones) or by increasing the proteostasis network capacity (proteostasis regulators). We propose that such therapeutic strategies, including combination therapies, represent a new approach for treating a range of diverse human maladies.
              Article 0 comments Cited 370 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Yuchen Guo:
                ORCID: https://orcid.org/0000-0002-2709-2713
                Journal
                Journal ID (nlm-ta): Stem Cells Int
                Journal ID (iso-abbrev): Stem Cells Int
                Journal ID (publisher-id): SCI
                Title: Stem Cells International
                Publisher: Hindawi
                ISSN (Print): 1687-966X
                ISSN (Electronic): 1687-9678
                Publication date Collection: 2020
                Publication date (Electronic): 8 July 2020
                Volume: 2020
                Electronic Location Identifier: 1047896
                Affiliations
                State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China
                Author notes

                Academic Editor: Yang Li

                Author information
                https://orcid.org/0000-0002-2709-2713
                Article
                DOI: 10.1155/2020/1047896
                PMC ID: 7366189
                PubMed ID: 32724310
                SO-VID: c49884a1-6699-445c-b16c-80c2cbc19bd6
                Copyright © Copyright © 2020 Shuang Jiang and Yuchen Guo.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 27 March 2020
                Date revision received : 11 June 2020
                Date accepted : 20 June 2020
                Funding
                Funded by: China Postdoctoral Science Foundation
                Award ID: 2019TQ0218
                Funded by: Sichuan University
                Award ID: RCDWJS2020-23
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Molecular medicine
                Data availability:
                ScienceOpen disciplines: Molecular medicine

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