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Studying Werner syndrome to elucidate mechanisms and therapeutics of human aging and age-related diseases | Biogerontology
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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 Alzheimerâs disease. Unraveling the sophisticated molecular mechanisms of the human aging process may provide novel strategies to extend âhealthy agingâ 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.
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pubmed, article, google, scholar, cas, syndrome, werner, central, aging, cell, dna, human, wrn, protein, bohr, helicase, oshima, gene, res, biol, genet, cells, ageing, stem, lebel, exonuclease, sci, research, fang, repair, replication, diseases, premature, elegans, nat, martin, mol, croteau, damage, zhang, model, mice, lee, disease, cancer, mutations, caenorhabditis, drosophila, exp, werners,
Topics {âď¸}
month download article/chapter double-strand dna breaks hoi-hung cheung genome-wide association study asian-ancestry samples identifies dna interstrand cross-links human aging-related diseases impaired protein-protein interactions brosh rm jr rothmund-thomson syndrome features hutchinsonâgilford progeria syndrome normal age-related diseases ethnic-specific alterations wrn-deficient human fibroblasts full article pdf caenorhabditis elegans mutant studying werner syndrome article biogerontology aims dominant human diseases dna damage induced gray md including caenorhabditis elegans additional information publisher' claudia piccoli privacy choices/manage cookies genetic alterations leading fang ef age-related diseases mason pa shen jc cellular werner phenotypes domenica caponio & evandro werner syndrome helicase werner syndrome protein rescue premature aging deficient dna repair stem cell model bloom syndrome protein werner helicase gene werner syndrome cells research grants council hydrogen sulfide restores werner syndrome gene distinct nuclear structures restores healthy aging article lautrup flies lacking wrn stem cell aging werner syndrome fibroblasts oxidative dna damage
Questions {â}
- Chang S (2005) A mouse model of Werner syndrome: what can it tell us about aging and cancer?
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headline:Studying Werner syndrome to elucidate mechanisms and therapeutics of human aging and age-related diseases
description: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 Alzheimerâs disease. Unraveling the sophisticated molecular mechanisms of the human aging process may provide novel strategies to extend âhealthy agingâ 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.
datePublished:2019-01-21T00:00:00Z
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Aging
Premature aging
Werner syndrome
NAD+
Mitophagy
Hallmarkers of aging
DNA repair
Cell Biology
Geriatrics/Gerontology
Developmental Biology
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headline:Studying Werner syndrome to elucidate mechanisms and therapeutics of human aging and age-related diseases
description: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 Alzheimerâs disease. Unraveling the sophisticated molecular mechanisms of the human aging process may provide novel strategies to extend âhealthy agingâ 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.
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Premature aging
Werner syndrome
NAD+
Mitophagy
Hallmarkers of aging
DNA repair
Cell Biology
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