Evidence map›Paper›PMID 34388363›Full record

ArticleStem cell reports2021

Sestrins regulate muscle stem cell metabolic homeostasis.

Benjamin A Yang, Jesus Castor-Macias, Paula Fraczek, Ashley Cornett, Lemuel A Brown, Myungjin Kim, Susan V Brooks, Isabelle M A Lombaert, Jun Hee Lee, Carlos A Aguilar

Abstract read
In one paragraph

Article in Stem cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Cellular mechanotransduction of human osteoblasts in microgravity.bioRxiv : the preprint server for biology · 2024
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Serum Sestrin-1 Concentration Is Higher in Frail than Non-Frail Older People Living in Nursing Homes.International journal of environmental research and public health · 2022
    Article
  15. The functions and roles of sestrins in regulating human diseases.Cellular & molecular biology letters · 2022
    Review
  16. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Benjamin A YangDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109, USA; Biointerfaces Institute, University of Michigan, Ann Arbor, MI 48109, USA.
Jesus Castor-MaciasDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109, USA; Biointerfaces Institute, University of Michigan, Ann Arbor, MI 48109, USA.
Paula FraczekDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109, USA; Biointerfaces Institute, University of Michigan, Ann Arbor, MI 48109, USA.
Ashley CornettBiointerfaces Institute, University of Michigan, Ann Arbor, MI 48109, USA; Biologic and Materials Sciences, School of Dentistry, University of Michigan, Ann Arbor, MI 48109, USA.
Lemuel A BrownDepartment of Molecular & Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA.
Myungjin KimDepartment of Molecular & Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA.
Susan V BrooksDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109, USA; Department of Molecular & Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA.
Isabelle M A LombaertBiointerfaces Institute, University of Michigan, Ann Arbor, MI 48109, USA; Biologic and Materials Sciences, School of Dentistry, University of Michigan, Ann Arbor, MI 48109, USA.
Jun Hee LeeDepartment of Molecular & Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA; Program in Cellular and Molecular Biology, University of Michigan, Ann Arbor, MI 48109, USA.
Carlos A AguilarDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109, USA; Biointerfaces Institute, University of Michigan, Ann Arbor, MI 48109, USA; Program in Cellular and Molecular Biology, University of Michigan, Ann Arbor, MI 48109, USA. Electronic address: caguilar@umich.edu.

Funding

Research Education CoreP30AG024824 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Neil Alexander · 2004 to 2026
$29.2M
Pilot and Feasibility (P and F) ProgramP30DK089503 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Joyce Lee · 2010 to 2026
$20.3M
PROJECT 3: Neuromuscular redox homeostasis in mice lacking SOD1 and aging wild type mice subcontract at University of LiverpoolP01AG051442 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI JACKSON, MALCOLM JOSEPH · 2016 to 2020
$8.9M
Structure, Composition, & Histology Core - Core BP30AR069620 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KARL J JEPSEN · 2016 to 2026
$8.4M
University of Michigan Postbaccalaureate Research Education Program (UM PREP)R25GM086262 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ALLEN, BENJAMIN · 2009 to 2024
$6.1M
GENETIC DETERMINATION OF SKELETAL FRAGILITYR01AR044927 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI JEPSEN, KARL J · 2002 to 2014
$4.3M
Microfluidics in Biomedical Sciences Training ProgramT32EB005582 · NIBIB · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FAN, XUDONG · 2005 to 2020
$3.9M
Bone Robustness as a Biomarker of Skeletal Aging and FragilityR01AR065424 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI JEPSEN, KARL J · 2014 to 2018
$2.4M
GENETIC DETERMINATION OF SKELETAL FRAGILITYR29AR044927 · NIAMS · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI JEPSEN, KARL J · 1998 to 2002
$268k
NIAMS NIH HHS P30 AR069620NIAMS NIH HHS R01 AR044927NIAMS NIH HHS R01 AR065424NIAMS NIH HHS R29 AR044927NIA NIH HHS P01 AG051442NIA NIH HHS P30 AG024824NIBIB NIH HHS T32 EB005582NIDDK NIH HHS P30 DK089503NIGMS NIH HHS R25 GM086262
6 · The paper itself

Abstract

The health and homeostasis of skeletal muscle are preserved by a population of tissue-resident muscle stem cells (MuSCs) that maintain a state of mitotic and metabolic quiescence in adult tissues. The capacity of MuSCs to preserve the quiescent state declines with aging and metabolic insults, promoting premature activation and stem cell exhaustion. Sestrins are a class of stress-inducible proteins that act as antioxidants and inhibit the activation of the mammalian target of rapamycin complex 1 (mTORC1) signaling complex. Despite these pivotal roles, the role of Sestrins has not been explored in adult stem cells. We show that SESTRIN1,2 loss results in hyperactivation of the mTORC1 complex, increased propensity to enter the cell cycle, and shifts in metabolic flux. Aged SESTRIN1,2 knockout mice exhibited loss of MuSCs and a reduced ability to regenerate injured muscle. These findings demonstrate that Sestrins help maintain metabolic pathways in MuSCs that protect quiescence against aging.

Indexed as

Energy MetabolismHomeostasisAge FactorsAnimalsBiomarkersCell Culture TechniquesCell SeparationGene Expression ProfilingGene Expression RegulationGene Knockdown TechniquesHigh-Throughput Nucleotide SequencingImmunohistochemistryImmunophenotypingMechanistic Target of Rapamycin Complex 1MiceMice, KnockoutBiomarkersMechanistic Target of Rapamycin Complex 1SestrinsagingmetabolismmTORC1oxidative stressreactive oxygen speciesregenerationRNA sequencingsatellite cells

Identifiers

PMID34388363
PMCPMC8452514

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.