Evidence map›Paper›PMID 41290624›Full record

ArticleNature communications2025

Non-canonical roles of Keap1/Nrf2 in regulating quiescence and early activation in adult muscle stem cells.

Lifang Han, Yudan Qiu, Liangqiang He, Chuan Gao, Nan Zhou, Xinrong Fu, Jingyan Xu, Lirong Lin, Huating Wang, Shyam Biswal and 1 more

Abstract read
In one paragraph

Article in Nature communications, 2025. 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. Veterinary sciences · 2026
    Article
  2. 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

11 authors.

Lifang HanDivision of Life Science and State Key Laboratory of Nervous System Disorders, Hong Kong University of Science & Technology, Kowloon, Hong Kong, China.ORCID http://orcid.org/0000-0001-8269-5114
Yudan QiuDivision of Life Science and State Key Laboratory of Nervous System Disorders, Hong Kong University of Science & Technology, Kowloon, Hong Kong, China.
Liangqiang HeDepartment of Orthopaedics and Traumatology, Li Ka Shing Institute of Health Sciences, Chinese University of Hong Kong, Shatin, Hong Kong, China.
Chuan GaoDivision of Life Science and State Key Laboratory of Nervous System Disorders, Hong Kong University of Science & Technology, Kowloon, Hong Kong, China.
Nan ZhouDivision of Life Science and State Key Laboratory of Nervous System Disorders, Hong Kong University of Science & Technology, Kowloon, Hong Kong, China.
Xinrong FuDivision of Life Science and State Key Laboratory of Nervous System Disorders, Hong Kong University of Science & Technology, Kowloon, Hong Kong, China.
Jingyan XuDivision of Life Science and State Key Laboratory of Nervous System Disorders, Hong Kong University of Science & Technology, Kowloon, Hong Kong, China.ORCID http://orcid.org/0000-0001-9109-5516
Lirong LinDivision of Life Science and State Key Laboratory of Nervous System Disorders, Hong Kong University of Science & Technology, Kowloon, Hong Kong, China.
Huating WangDepartment of Orthopaedics and Traumatology, Li Ka Shing Institute of Health Sciences, Chinese University of Hong Kong, Shatin, Hong Kong, China.ORCID http://orcid.org/0000-0001-5474-2905
Shyam BiswalDepartment of Environmental Health and Engineering, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA.
Zhenguo WuDivision of Life Science and State Key Laboratory of Nervous System Disorders, Hong Kong University of Science & Technology, Kowloon, Hong Kong, China. bczgwu@ust.hk.ORCID http://orcid.org/0000-0003-3049-8324

Funding

Innovation and Technology Commission (ITF) ITCPD/17-9Research Grants Council, University Grants Committee (RGC, UGC) AoE/M-09/12Research Grants Council, University Grants Committee (RGC, UGC) AoE/M-604/16Research Grants Council, University Grants Committee (RGC, UGC) C6018-19GResearch Grants Council, University Grants Committee (RGC, UGC) GRF16103220Research Grants Council, University Grants Committee (RGC, UGC) T13-605/18-W
6 · The paper itself

Abstract

Adult muscle satellite cells (MuSCs) are mostly quiescent in uninjured muscles under normal homeostasis. Although several mechanisms underlying quiescence maintenance are known, our understanding of the process remains incomplete. Here, we show that Keap1 regulates MuSC quiescence maintenance by promoting Nrf2 protein degradation. Inducible deletion of Keap1 activates MuSCs to different extent in a sex-specific manner via differential Nrf2 protein levels: in Keap1-null MuSCs from male mice, Nrf2 protein is at an intermediate level due to the action of a GSK3β-dependent Nrf2 degradation system, which promotes mutant MuSCs to enter a G

Indexed as

Adult Stem CellsKelch-Like ECH-Associated Protein 1NF-E2-Related Factor 2Satellite Cells, Skeletal MuscleAnimalsFemaleGlycogen Synthase Kinase 3 betaMaleMiceMice, Inbred C57BLMice, KnockoutMuscle, SkeletalGlycogen Synthase Kinase 3 betaKeap1 protein, mouseKelch-Like ECH-Associated Protein 1Nfe2l2 protein, mouseNF-E2-Related Factor 2

Identifiers

PMID41290624
PMCPMC12647642

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.