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nature portfolio privacy policy acetylation/deacetylation-dependent nucleo-cytoplasmic transport double-strand break repair/dsbr nad+-sirt1-pgc1α-dependent mitochondrial biogenesis advertising programming language poly-l-lysine-coated slides double-strand dna breaks validate ms/ms-based peptide reprints fat-metabolism-related molecular pathways57 fat-metabolism/catabolism-related proteins lc-ms/ms-based par quantification rad-51-positive foci/mitotic region transformative cancer research nature 568 nature 521 nature 508 nature 536 nature 528 nature 543 nature thermo fisher scientific real-time quantitative pcr fat-metabolism-related molecular pathways german research foundation free access ho-joon lee base excision repair/ber martin borch jensen intramural research program key metabolic sensor/regulator anti-aging molecule nad+ nad-dependent deacetylase sirt1 full size image liquid chromatography-mass spectrometry calorie-restricted caenorhabditis elegans glutamine-dependent nad+ synthetase15 kaplan–meier survival curves mitophagy inhibits amyloid-beta national research council sun yat-sen university age-related metabolic outcomes nad+-ampk-ulk1-mitophagy pathway hot ethanol/hepes buffer 1x phosphate-buffered saline d3- methyl-4-pyridone-3-carboxamide original author nad+/sirtuins-ampk-ulk1 pathway

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         headline:NAD+ augmentation restores mitophagy and limits accelerated aging in Werner syndrome
         description:Metabolic dysfunction is a primary feature of Werner syndrome (WS), a human premature aging disease caused by mutations in the gene encoding the Werner (WRN) DNA helicase. WS patients exhibit severe metabolic phenotypes, but the underlying mechanisms are not understood, and whether the metabolic deficit can be targeted for therapeutic intervention has not been determined. Here we report impaired mitophagy and depletion of NAD+, a fundamental ubiquitous molecule, in WS patient samples and WS invertebrate models. WRN regulates transcription of a key NAD+ biosynthetic enzyme nicotinamide nucleotide adenylyltransferase 1 (NMNAT1). NAD+ repletion restores NAD+ metabolic profiles and improves mitochondrial quality through DCT-1 and ULK-1-dependent mitophagy. At the organismal level, NAD+ repletion remarkably extends lifespan and delays accelerated aging, including stem cell dysfunction, in Caenorhabditis elegans and Drosophila melanogaster models of WS. Our findings suggest that accelerated aging in WS is mediated by impaired mitochondrial function and mitophagy, and that bolstering cellular NAD+ levels counteracts WS phenotypes. The molecular mechanisms of mitochondrial dysfunction in the premature ageing Werner syndrome were elusive. Here the authors show that NAD+ depletion-induced impaired mitophagy contributes to this phenomenon, shedding light on potential therapeutics.
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      headline:NAD+ augmentation restores mitophagy and limits accelerated aging in Werner syndrome
      description:Metabolic dysfunction is a primary feature of Werner syndrome (WS), a human premature aging disease caused by mutations in the gene encoding the Werner (WRN) DNA helicase. WS patients exhibit severe metabolic phenotypes, but the underlying mechanisms are not understood, and whether the metabolic deficit can be targeted for therapeutic intervention has not been determined. Here we report impaired mitophagy and depletion of NAD+, a fundamental ubiquitous molecule, in WS patient samples and WS invertebrate models. WRN regulates transcription of a key NAD+ biosynthetic enzyme nicotinamide nucleotide adenylyltransferase 1 (NMNAT1). NAD+ repletion restores NAD+ metabolic profiles and improves mitochondrial quality through DCT-1 and ULK-1-dependent mitophagy. At the organismal level, NAD+ repletion remarkably extends lifespan and delays accelerated aging, including stem cell dysfunction, in Caenorhabditis elegans and Drosophila melanogaster models of WS. Our findings suggest that accelerated aging in WS is mediated by impaired mitochondrial function and mitophagy, and that bolstering cellular NAD+ levels counteracts WS phenotypes. The molecular mechanisms of mitochondrial dysfunction in the premature ageing Werner syndrome were elusive. Here the authors show that NAD+ depletion-induced impaired mitophagy contributes to this phenomenon, shedding light on potential therapeutics.
      datePublished:2019-11-21T00:00:00Z
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               type:PostalAddress
            type:Organization
            name:University of Copenhagen
            address:
               name:Danish Center for Healthy Aging, University of Copenhagen, Copenhagen, Denmark
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, USA
      name:Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lørenskog, Norway
      name:Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, USA
      name:Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lørenskog, Norway
      name:Buck Institute for Research on Aging, Novato, USA
      name:Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, USA
      name:Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lørenskog, Norway
      name:Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lørenskog, Norway
      name:Department of Molecular Cell Biology, Institute for Cancer Research, Oslo University Hospital, Montebello, Norway
      name:Centre for Cancer Biomedicine, Faculty of Medicine, University of Oslo, Montebello, Norway
      name:Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, USA
      name:Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Baltimore, USA
      name:Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lørenskog, Norway
      name:Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, USA
      name:Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, USA
      name:Danish Center for Healthy Aging, University of Copenhagen, Copenhagen, Denmark
      name:Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, USA
      name:Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Chuo-ku, Japan
      name:Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, USA
      name:Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lørenskog, Norway
      name:Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, USA
      name:Molecular Toxicology Group, Department of Biology, University of Konstanz, Konstanz, Germany
      name:Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, USA
      name:Molecular Toxicology Group, Department of Biology, University of Konstanz, Konstanz, Germany
      name:Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, USA
      name:Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Chuo-ku, Japan
      name:Department of Molecular and Integrative Physiology, and Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, USA
      name:Department of Hypertension and Vascular Disease, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China
      name:Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Chuo-ku, Japan
      name:Department of Molecular Cell Biology, Institute for Cancer Research, Oslo University Hospital, Montebello, Norway
      name:Centre for Cancer Biomedicine, Faculty of Medicine, University of Oslo, Montebello, Norway
      name:Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Baltimore, USA
      name:Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, USA
      name:Buck Institute for Research on Aging, Novato, USA
      name:Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lørenskog, Norway
      name:Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, USA
      name:Danish Center for Healthy Aging, University of Copenhagen, Copenhagen, Denmark

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