Evidence map›Paper›PMID 41456123›Full record

ArticleAutophagy2026

DEAF1 - a transcriptional brake on muscle autophagy.

Wen Xing Lee, Kah Yong Goh, Sze Mun Choy, Hong-Wen Tang

Abstract read
In one paragraph

Article in Autophagy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

4 authors.

Wen Xing LeeProgram in Cancer and Stem Cell Biology, Duke-NUS Medical School, Singapore, Singapore.
Kah Yong GohProgram in Cancer and Stem Cell Biology, Duke-NUS Medical School, Singapore, Singapore.
Sze Mun ChoyProgram in Cancer and Stem Cell Biology, Duke-NUS Medical School, Singapore, Singapore.
Hong-Wen TangProgram in Cancer and Stem Cell Biology, Duke-NUS Medical School, Singapore, Singapore.ORCID 0000-0002-8347-9891

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macroautophagy/autophagy protects muscle from proteotoxic stress and maintains tissue homeostasis, yet skeletal muscle relies on it more than most organs. Adult fibers endure constant mechanical strain and require continuous turnover of long-lived proteins, while muscle stem cells (MuSCs) depend on autophagy to remain quiescent, activate after injury, and regenerate effectively. How autophagy is transcriptionally regulated in muscle has been unclear. We identified DEAF1 as a transcriptional brake on autophagy. In MuSCs, DEAF1 controls activation and regeneration and becomes aberrantly elevated with age, promoting protein aggregate formation and cell death. In muscle fibers, DEAF1 is chronically induced during aging, suppressing autophagy and driving functional decline. Exercise reverses DEAF1 induction, restoring autophagy and muscle function. These findings reveal DEAF1 as a key regulator linking autophagy to regeneration and aging, highlighting a therapeutically tractable axis for preserving muscle health.

Indexed as

AutophagyMuscle, SkeletalTranscription, GeneticAgingAnimalsHumansMiceRegenerationAutophagyDEAF1musclemuscle stem cellregeneration

Identifiers

PMID41456123
PMCPMC13048571

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.