Evidence map›Paper›PMID 41610257›Full record

ArticleScience (New York, N.Y.)2026

Cellular survivorship bias as a mechanistic driver of muscle stem cell aging.

Jengmin Kang, Daniel I Benjamin, Qiqi Guo, Chauncey Evangelista, Soochi Kim, Marina Arjona, Pieter Both, Mingyu Chung, Ananya K Krishnan, Gurkamal Dhaliwal and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Science (New York, N.Y.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Review
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

12 authors.

Jengmin Kang *Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0002-5539-3070
Daniel I Benjamin *Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Qiqi GuoBroad Stem Cell Research Center, University of California Los Angeles, Los Angeles, CA, USA.
Chauncey EvangelistaBroad Stem Cell Research Center, University of California Los Angeles, Los Angeles, CA, USA.
Soochi KimDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0003-2054-6097
Marina ArjonaDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Pieter BothDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Mingyu ChungDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0003-1718-6203
Ananya K KrishnanDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0003-2850-9741
Gurkamal DhaliwalDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0009-0002-6290-8957
Richard LamDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0009-0004-8315-7843
Thomas A RandoDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0001-5843-8564

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
Genomic Instability as A Driver of Stem Cell ExhaustionR01AG082764 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI THOMAS A. RANDO · 2023 to 2026
$1.7M
NIA NIH HHS P01 AG036695NIA NIH HHS R01 AG068667NIA NIH HHS R01 AG082764
6 · The paper itself

Abstract

Aging is characterized by a decline in the ability of tissue repair and regeneration after injury. In skeletal muscle, this decline is largely driven by impaired function of muscle stem cells (MuSCs) to efficiently contribute to muscle regeneration. We uncovered a cause of this aging-associated dysfunction: a cellular survivorship bias that prioritizes stem cell persistence at the expense of functionality. With age, MuSCs increased expression of a tumor suppressor, N-myc down-regulated gene 1 (NDRG1), which, by suppressing the mammalian target of rapamycin (mTOR) pathway, increased their long-term survival potential but at the cost of their ability to promptly activate and contribute to muscle regeneration. This delayed muscle regeneration with age may result from a trade-off that favors long-term stem cell survival over immediate regenerative capacity.

Indexed as

AgingCellular SenescenceMuscle, SkeletalRegenerationSatellite Cells, Skeletal MuscleAnimalsCell Cycle ProteinsCell SurvivalIntracellular Signaling Peptides and ProteinsMiceTOR Serine-Threonine KinasesCell Cycle ProteinsIntracellular Signaling Peptides and ProteinsmTOR protein, mouseTOR Serine-Threonine Kinases

Identifiers

PMID41610257
PMCPMC12981041

What OpenQuestion holds

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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.