ArticleCell metabolism2023
Multiomics reveals glutathione metabolism as a driver of bimodality during stem cell aging.
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Article in Cell metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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37 citing papers in PubMed, 68 citations in OpenAlex.
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Authors and funding
17 authors at 3 institutions in 1 country.
Daniel I BenjaminDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA; Paul F. Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA, USA.
Jamie O BrettDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA; Paul F. Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA, USA; Stem Cell Biology and Regenerative Medicine Graduate Program, Stanford University School of Medicine, Stanford, CA, USA; Medical Scientist Training Program, Stanford University School of Medicine, Stanford, CA, USA.
Pieter BothDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA; Paul F. Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA, USA; Stem Cell Biology and Regenerative Medicine Graduate Program, Stanford University School of Medicine, Stanford, CA, USA.
Joel S BenjaminDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA; Paul F. Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA, USA.
Heather L IshakPaul F. Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA, USA.
Jengmin KangDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA; Paul F. Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA, USA.
Soochi KimDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA; Paul F. Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA, USA.
Mingyu ChungDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA; Paul F. Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA, USA.
Marina ArjonaDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA; Paul F. Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA, USA.
Christopher W NutterPaul F. Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA, USA.
Jenna H TanPaul F. Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA, USA.
Ananya K KrishnanPaul F. Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA, USA.
Hunter DulayPaul F. Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA, USA.
Sharon M LouieDepartment of Nutritional Sciences and Toxicology, University of California, Berkeley, Berkeley, CA 94720, USA.
Antoine de MorreeDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA; Paul F. Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA, USA.
Daniel K NomuraDepartment of Nutritional Sciences and Toxicology, University of California, Berkeley, Berkeley, CA 94720, USA.
Thomas A RandoDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA; Paul F. Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA, USA; Neurology Service, Veterans Affairs Palo Alto Healthcare System, Palo Alto, CA, USA. Electronic address: trando@mednet.ucla.edu.
Stanford University · USUniversity of California, Berkeley · USVA Palo Alto Health Care System · US
Funding
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007365 · NIGMS · STANFORD UNIVERSITY · PI CHUA, KATRIN F · 1985 to 2021
$33.8MWnt signaling in muscle stem cell agingP01AG036695 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MARGARET A. GOODELL · 2011 to 2026
$29.3MTraining in Basic Research on Aging and Age-Related DiseaseT32AG000266 · NIA · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI Lisa M Ellerby · 1998 to 2026
$13.8MNotch Signaling and Satellite Cell ActivationR37AG023806 · NIA · STANFORD UNIVERSITY · PI RANDO, THOMAS A. · 2010 to 2019
$2.9MAging and Stem Cell ResilienceR01AG068667 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI RANDO, THOMAS A. · 2021 to 2025
$2.8MMolecular Regulation of Stem Cell QuiescenceR01AR073248 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI RANDO, THOMAS A. · 2018 to 2022
$2.6MEpigenetic Reprogramming of Cellular AgeR01AG071783 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI RANDO, THOMAS A. · 2021 to 2025
$2.2MThe Function and Regulation of Pax3 in Muscle Stem CellsR01AR062185 · NIAMS · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI RANDO, THOMAS A. · 2011 to 2015
$1.5MRegulation of Muscle Fibrosis in Response to Injury and AgingI01BX002324 · VA · VETERANS ADMIN PALO ALTO HEALTH CARE SYS · PI RANDO, THOMAS A. · 2014 to 2021
–BLRD VA I01 BX002324NIAMS NIH HHS R01 AR062185NIAMS NIH HHS R01 AR073248NIA NIH HHS P01 AG036695NIA NIH HHS R01 AG068667NIA NIH HHS R01 AG071783NIA NIH HHS R37 AG023806NIA NIH HHS T32 AG000266NIGMS NIH HHS T32 GM007365
Abstract
With age, skeletal muscle stem cells (MuSCs) activate out of quiescence more slowly and with increased death, leading to defective muscle repair. To explore the molecular underpinnings of these defects, we combined multiomics, single-cell measurements, and functional testing of MuSCs from young and old mice. The multiomics approach allowed us to assess which changes are causal, which are compensatory, and which are simply correlative. We identified glutathione (GSH) metabolism as perturbed in old MuSCs, with both causal and compensatory components. Contrary to young MuSCs, old MuSCs exhibit a population dichotomy composed of GSH
Indexed as
MultiomicsMuscle, SkeletalAgingAnimalsCellular SenescenceMiceStem CellsagingbimodalityGSHmultiomicsMuSCNACsatellite cellsstem cells
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