Model of human aging: Recent findings on Werner’s and Hutchinson-Gilford progeria syndromes

Model of human aging: Recent findings on Werner’s and Hutchinson-Gilford progeria syndromes

Shian-ling Ding1, Chen-Yang Shen2,3,41Department of Nursing, Kang-Ning Junior College of Medical Care and Management, Taipei, Taiwan; 2Institute of Biomedical Sciences, and 3Life Science Library, Academia Sinica, Taipei, Taiwan; 4Graduate Institute of Environmental Science, China Medical University,...

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Autores principales: Shian-ling Ding, Chen-Yang Shen
Formato: article
Lenguaje:EN
Publicado: Dove Medical Press 2008
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Geriatrics
RC952-954.6
Acceso en línea:https://doaj.org/article/89de1282401f49f181bb7ea3ebb39c34
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spelling oai:doaj.org-article:89de1282401f49f181bb7ea3ebb39c342021-12-02T06:51:17ZModel of human aging: Recent findings on Werner’s and Hutchinson-Gilford progeria syndromes1178-1998https://doaj.org/article/89de1282401f49f181bb7ea3ebb39c342008-09-01T00:00:00Zhttps://www.dovepress.com/model-of-human-aging-recent-findings-on-wernerrsquos-and-hutchinson-gi-peer-reviewed-article-CIAhttps://doaj.org/toc/1178-1998Shian-ling Ding1, Chen-Yang Shen2,3,41Department of Nursing, Kang-Ning Junior College of Medical Care and Management, Taipei, Taiwan; 2Institute of Biomedical Sciences, and 3Life Science Library, Academia Sinica, Taipei, Taiwan; 4Graduate Institute of Environmental Science, China Medical University, Taichong, TaiwanAbstract: The molecular mechanisms involved in human aging are complicated. Two progeria syndromes, Werner’s syndrome (WS) and Hutchinson-Gilford progeria syndrome (HGPS), characterized by clinical features mimicking physiological aging at an early age, provide insights into the mechanisms of natural aging. Based on recent findings on WS and HGPS, we suggest a model of human aging. Human aging can be triggered by two main mechanisms, telomere shortening and DNA damage. In telomere-dependent aging, telomere shortening and dysfunction may lead to DNA damage responses which induce cellular senescence. In DNA damage-initiated aging, DNA damage accumulates, along with DNA repair deficiencies, resulting in genomic instability and accelerated cellular senescence. In addition, aging due to both mechanisms (DNA damage and telomere shortening) is strongly dependent on p53 status. These two mechanisms can also act cooperatively to increase the overall level of genomic instability, triggering the onset of human aging phenotypes.Keywords: human aging, Hutchinson-Gilford Progeria syndrome, Werner syndromeShian-ling DingChen-Yang ShenDove Medical PressarticleGeriatricsRC952-954.6ENClinical Interventions in Aging, Vol Volume 3, Pp 431-444 (2008)
institution DOAJ
collection DOAJ
language EN
topic Geriatrics
RC952-954.6
spellingShingle Geriatrics
RC952-954.6
Shian-ling Ding
Chen-Yang Shen
Model of human aging: Recent findings on Werner’s and Hutchinson-Gilford progeria syndromes
description Shian-ling Ding1, Chen-Yang Shen2,3,41Department of Nursing, Kang-Ning Junior College of Medical Care and Management, Taipei, Taiwan; 2Institute of Biomedical Sciences, and 3Life Science Library, Academia Sinica, Taipei, Taiwan; 4Graduate Institute of Environmental Science, China Medical University, Taichong, TaiwanAbstract: The molecular mechanisms involved in human aging are complicated. Two progeria syndromes, Werner’s syndrome (WS) and Hutchinson-Gilford progeria syndrome (HGPS), characterized by clinical features mimicking physiological aging at an early age, provide insights into the mechanisms of natural aging. Based on recent findings on WS and HGPS, we suggest a model of human aging. Human aging can be triggered by two main mechanisms, telomere shortening and DNA damage. In telomere-dependent aging, telomere shortening and dysfunction may lead to DNA damage responses which induce cellular senescence. In DNA damage-initiated aging, DNA damage accumulates, along with DNA repair deficiencies, resulting in genomic instability and accelerated cellular senescence. In addition, aging due to both mechanisms (DNA damage and telomere shortening) is strongly dependent on p53 status. These two mechanisms can also act cooperatively to increase the overall level of genomic instability, triggering the onset of human aging phenotypes.Keywords: human aging, Hutchinson-Gilford Progeria syndrome, Werner syndrome
format article
author Shian-ling Ding
Chen-Yang Shen
author_facet Shian-ling Ding
Chen-Yang Shen
author_sort Shian-ling Ding
title Model of human aging: Recent findings on Werner’s and Hutchinson-Gilford progeria syndromes
title_short Model of human aging: Recent findings on Werner’s and Hutchinson-Gilford progeria syndromes
title_full Model of human aging: Recent findings on Werner’s and Hutchinson-Gilford progeria syndromes
title_fullStr Model of human aging: Recent findings on Werner’s and Hutchinson-Gilford progeria syndromes
title_full_unstemmed Model of human aging: Recent findings on Werner’s and Hutchinson-Gilford progeria syndromes
title_sort model of human aging: recent findings on werner’s and hutchinson-gilford progeria syndromes
publisher Dove Medical Press
publishDate 2008
url https://doaj.org/article/89de1282401f49f181bb7ea3ebb39c34
work_keys_str_mv AT shianlingding modelofhumanagingrecentfindingsonwernerrsquosandhutchinsongilfordprogeriasyndromes
AT chenyangshen modelofhumanagingrecentfindingsonwernerrsquosandhutchinsongilfordprogeriasyndromes
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