Evidence map›Paper›PMID 38243132›Full record

ArticleNature metabolism2024

Depletion of SAM leading to loss of heterochromatin drives muscle stem cell ageing.

Jengmin Kang, Daniel I Benjamin, Soochi Kim, Jayesh S Salvi, Gurkamal Dhaliwal, Richard Lam, Armon Goshayeshi, Jamie O Brett, Ling Liu, Thomas A Rando

Open access · greenAbstract read
In one paragraph

Article in Nature metabolism, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
11.9field-weighted citation impact, top 1% of its field
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

45 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Maternal methionine supplementation regulates skeletal muscle development through NAnimal nutrition (Zhongguo xu mu shou yi xue hui) · 2026
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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 at 2 institutions in 1 country.

Jengmin KangDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID http://orcid.org/0000-0002-5539-3070
Daniel I BenjaminDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Soochi KimDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Jayesh S SalviDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID http://orcid.org/0000-0003-1122-239X
Gurkamal DhaliwalPaul F. Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA, USA.ORCID http://orcid.org/0009-0002-6290-8957
Richard LamPaul F. Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA, USA.ORCID http://orcid.org/0009-0004-8315-7843
Armon GoshayeshiPaul F. Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA, USA.ORCID http://orcid.org/0000-0003-4879-1916
Jamie O BrettDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID http://orcid.org/0000-0003-3112-5204
Ling LiuDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID http://orcid.org/0000-0002-0496-9551
Thomas A RandoDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA. trando@mednet.ucla.edu.ORCID http://orcid.org/0000-0001-5843-8564
Stanford University · USUniversity of California, Los Angeles · US

Funding

Wnt signaling in muscle stem cell agingP01AG036695 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MARGARET A. GOODELL · 2011 to 2026
$29.3M
Aging and Stem Cell ResilienceR01AG068667 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI RANDO, THOMAS A. · 2021 to 2025
$2.8M
Molecular Regulation of Stem Cell QuiescenceR01AR073248 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI RANDO, THOMAS A. · 2018 to 2022
$2.6M
Epigenetic Reprogramming of Cellular AgeR01AG071783 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI RANDO, THOMAS A. · 2021 to 2025
$2.2M
Genomic Instability as A Driver of Stem Cell ExhaustionR01AG082764 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI THOMAS A. RANDO · 2023 to 2026
$1.7M
Ultra high throughput sequencer for sustaining and enhancing multi-scale genomic studiesS10OD025212 · OD · STANFORD UNIVERSITY · PI SNYDER, MICHAEL P. · 2018 to 2018
$600k
Xevo TQ-XS Triple Quadrupole Mass Spectrometer SystemS10OD026962 · OD · STANFORD UNIVERSITY · PI CHIEN, ALLIS SOE-LANG · 2019 to 2019
$527k
Computer ClusterS10OD021763 · OD · STANFORD UNIVERSITY · PI JI, HANLEE P · 2016 to 2016
$481k
OneView 4kX4k sCMOS camera for transmission electron microscopy applicationsS10OD028536 · OD · STANFORD UNIVERSITY · PI MULHOLLAND, JONATHAN W · 2020 to 2020
$195k
NIAMS NIH HHS R01 AR073248NIA NIH HHS P01 AG036695NIA NIH HHS R01 AG068667NIA NIH HHS R01 AG071783NIA NIH HHS R01 AG082764NIH HHS S10 OD021763NIH HHS S10 OD025212NIH HHS S10 OD026962NIH HHS S10 OD028536
6 · The paper itself

Abstract

The global loss of heterochromatin during ageing has been observed in eukaryotes from yeast to humans, and this has been proposed as one of the causes of ageing. However, the cause of this age-associated loss of heterochromatin has remained enigmatic. Here we show that heterochromatin markers, including histone H3K9 di/tri-methylation and HP1, decrease with age in muscle stem cells (MuSCs) as a consequence of the depletion of the methyl donor S-adenosylmethionine (SAM). We find that restoration of intracellular SAM in aged MuSCs restores heterochromatin content to youthful levels and rejuvenates age-associated features, including DNA damage accumulation, increased cell death, and defective muscle regeneration. SAM is not only a methyl group donor for transmethylation, but it is also an aminopropyl donor for polyamine synthesis. Excessive consumption of SAM in polyamine synthesis may reduce its availability for transmethylation. Consistent with this premise, we observe that perturbation of increased polyamine synthesis by inhibiting spermidine synthase restores intracellular SAM content and heterochromatin formation, leading to improvements in aged MuSC function and regenerative capacity in male and female mice. Together, our studies demonstrate a direct causal link between polyamine metabolism and epigenetic dysregulation during murine MuSC ageing.

Indexed as

HeterochromatinS-AdenosylmethionineAgedAgingAnimalsCellular SenescenceFemaleHumansMaleMiceMusclesPolyaminesHeterochromatinPolyaminesS-Adenosylmethionine

Identifiers

PMID38243132
PMCPMC10976122
OpenAlexW4391027809

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.