Evidence map›Paper›PMID 42752358›Full record

ArticleeLife2026

Synergistic inhibition of Notch signaling and forced cell cycle re-entry drive Müller glia reprogramming in uninjured mouse retina.

Baoshan Liao, Chengshang Lyu, Yuqing Jiang, Shanggong Liu, Waiho Wong, Jiadong Zhang, Hoyin Tsang, Junxi Xie, Lingxi Chen, Qinrong Zhang and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in eLife, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

11 authors.

Baoshan LiaoDepartment of Biomedical Sciences, College of Biomedicine, City University of Hong Kong, Hong Kong, China.ORCID https://orcid.org/0009-0007-6599-624X
Chengshang LyuDepartment of Biomedical Sciences, College of Biomedicine, City University of Hong Kong, Hong Kong, China.ORCID https://orcid.org/0000-0002-0971-2851
Yuqing JiangDepartment of Biomedical Sciences, College of Biomedicine, City University of Hong Kong, Hong Kong, China.
Shanggong LiuDepartment of Biomedical Sciences, College of Biomedicine, City University of Hong Kong, Hong Kong, China.
Waiho WongDepartment of Biomedical Sciences, College of Biomedicine, City University of Hong Kong, Hong Kong, China.
Jiadong ZhangDepartment of Biomedical Engineering, College of Biomedicine, City University of Hong Kong, Hong Kong, China.
Hoyin TsangDepartment of Biomedical Sciences, College of Biomedicine, City University of Hong Kong, Hong Kong, China.
Junxi XieDepartment of Biomedical Sciences, College of Biomedicine, City University of Hong Kong, Hong Kong, China.
Lingxi ChenDepartment of Biomedical Sciences, College of Biomedicine, City University of Hong Kong, Hong Kong, China.
Qinrong ZhangDepartment of Biomedical Engineering, College of Biomedicine, City University of Hong Kong, Hong Kong, China.ORCID https://orcid.org/0000-0001-8893-514X
Wenjun XiongDepartment of Biomedical Sciences, College of Biomedicine, City University of Hong Kong, Hong Kong, China.ORCID https://orcid.org/0000-0001-6836-2807

Funding

Health and Medical Research Fund 05160276Health and Medical Research Fund 06172466Research Grants Council, University Grants Committee 11100723Research Grants Council, University Grants Committee 11102922Research Grants Council, University Grants Committee 11103819
6 · The paper itself

Abstract

In regenerative species, such as teleost fish, Müller glia (MG) autonomously re-enter the cell cycle after injury and give rise to functional retinal neurons. In contrast, the loss of retinal neurons in mammals is irreversible due to the limited proliferative and regenerative ability of MG. Various strategies have been developed to induce proliferation of mature mouse MG with or without injury, yet most MG daughter cells retain glial cell fate. Here, we found that MG progenies maintain high Notch signaling, which may constrain their neurogenic potential. Conditional deletion of

Indexed as

Cell CycleEpendymoglial CellsReceptors, NotchRetinaSignal TransductionAnimalsCell DifferentiationCell ProliferationCyclin D1Cyclin-Dependent Kinase Inhibitor p27Immunoglobulin J Recombination Signal Sequence-Binding ProteinMiceCcnd1 protein, mouseCdkn1b protein, mouseCyclin D1Cyclin-Dependent Kinase Inhibitor p27Immunoglobulin J Recombination Signal Sequence-Binding ProteinRbpj protein, mouseReceptors, NotchdifferentiationmouseMüller glianotchregenerationregenerative medicineretinaretinal cell differentiationstem cells

Identifiers

PMID42752358
PMCPMC13585425

What Socratic holds

Textmetadata
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.