Studying Werner syndrome to elucidate mechanisms and therapeutics of human aging and age-related diseases

Sofie Lautrup, Domenica Caponio, Hoi Hung Cheung, Claudia Piccoli, Tinna Stevnsner, Wai Yee Chan, Evandro F. Fang*

*Corresponding author for this work

    Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperReviewResearchpeer-review

    Abstract

    Aging is a natural and unavoidable part of life. However, aging is also the primary driver of the dominant human diseases, such as cardiovascular disease, cancer, and neurodegenerative diseases, including Alzheimer’s disease. Unraveling the sophisticated molecular mechanisms of the human aging process may provide novel strategies to extend ‘healthy aging’ and the cure of human aging-related diseases. Werner syndrome (WS), is a heritable human premature aging disease caused by mutations in the gene encoding the Werner (WRN) DNA helicase. As a classical premature aging disease, etiological exploration of WS can shed light on the mechanisms of normal human aging and facilitate the development of interventional strategies to improve healthspan. Here, we summarize the latest progress of the molecular understandings of WRN protein, highlight the advantages of using different WS model systems, including Caenorhabditis elegans, Drosophila melanogaster and induced pluripotent stem cell (iPSC) systems. Further studies on WS will propel drug development for WS patients, and possibly also for normal age-related diseases.

    Original languageEnglish
    JournalBiogerontology
    Volume20
    Issue3
    Pages (from-to)255-269
    Number of pages15
    ISSN1389-5729
    DOIs
    Publication statusPublished - Jun 2019

    Keywords

    • Aging
    • DNA repair
    • Hallmarkers of aging
    • Mitophagy
    • NAD
    • Premature aging
    • Werner syndrome
    • VITAMIN-C
    • LIFE-SPAN
    • SYNDROME FIBROBLASTS
    • DNA-DAMAGE
    • DOWN-REGULATION
    • SYNDROME PROTEIN
    • ELEGANS WRN HELICASE
    • NUCLEAR-LOCALIZATION
    • GENE
    • NAD(+)
    • STEM-CELL MODEL

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