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What can we learn from Werner syndrome? A biased view from a rheumatologist

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  • Published:
Modern Rheumatology

Abstract

 Werner syndrome (WS), caused by the mutation of the RecQ3 DNA helicase gene (loss of function), manifests scleroderma-like skin changes and juvenile cataracts in addition to a variety of clinical and biochemical aging phenotypes at an early stage of life, followed by death at an average age of 46 years. WS has been nominated as a top-ranking premature aging syndrome, or a human model of accelerated aging. Analyses of clinical and biological deterioration of body systems observed in WS may shed a unique light on the role of gene(s) in the pathogenesis of systemic sclerosis (SSc) and normal human aging.

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Authors and Affiliations

  1. Department of Rheumatology, Tokyo Metropolitan Ohtsuka Hospital, 2-8-1 Minami-Otsuka, Toshima-ku, Tokyo 170-0005, Japan Tel. +81-3-3941-3211; Fax +81-3-3941-7267 e-mail: m.goto-o@ohtsuka-hospital.toshima.tokyo.jp, , , , , , JP

    M. Goto

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  1. M. Goto
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Correspondence to:M. Goto

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Goto, M. What can we learn from Werner syndrome? A biased view from a rheumatologist. Mod Rheumatol 12, 0294–0299 (2002). https://doi.org/10.1007/s101650200052

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  • DOI: https://doi.org/10.1007/s101650200052

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