Evidence map›Paper›PMID 41912102›Full record

ArticlePharmacological research2026

Isoginkgetin protects against degeneration of ALS motor neurons via regulating the GSK-3β-TFEB signaling axis.

Ang Li, Xianglu Xiao, Guopan Liu, Krinos Li, Yixia Ling, Shenglong Deng, Chunzuan Xu, Shu-Qin Cao, Jing Wen, Guang Lu and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Pharmacological research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. 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

14 authors.

Ang LiState Key Laboratory of Mechanism and Quality of Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.
Xianglu XiaoBioengineering Department and Imperial-X, Imperial College London, London W12 7SL, United Kingdom.
Guopan LiuGuangdong Engineering Technology Research Center of Biological Targeting Diagnosis, Therapy and Rehabilitation, The Fifth Affiliated Hospital, Guangzhou Medical University, No.621 Gangwan Road, Guangzhou, China; Centre for Regenerative Medicine and Health, Hong Kong Institute of Science & Innovation, Chinese Academy of Sciences, Hong Kong, China.
Krinos LiBioengineering Department and Imperial-X, Imperial College London, London W12 7SL, United Kingdom.
Yixia LingGuangdong Engineering Technology Research Center of Biological Targeting Diagnosis, Therapy and Rehabilitation, The Fifth Affiliated Hospital, Guangzhou Medical University, No.621 Gangwan Road, Guangzhou, China.
Shenglong DengBioengineering Department and Imperial-X, Imperial College London, London W12 7SL, United Kingdom.
Chunzuan XuState Key Laboratory of Mechanism and Quality of Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.
Shu-Qin CaoDepartment of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lørenskog 1478, Norway.
Jing WenState Key Laboratory of Mechanism and Quality of Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.
Guang LuDepartment of Physiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Guang YangBioengineering Department and Imperial-X, Imperial College London, London W12 7SL, United Kingdom; National Heart and Lung Institute, Imperial College London, London SW7 2AZ, United Kingdom; Cardiovascular Research Centre, Royal Brompton Hospital, London SW3 6NP, United Kingdom; School of Biomedical Engineering & Imaging Sciences, King's College London, London WC2R 2LS, United Kingdom.
Evandro F FangDepartment of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lørenskog 1478, Norway; The Norwegian Centre on Healthy Ageing (NO-Age) and the Norwegian National anti-Alzheimer's Disease (NO-AD) Networks, Oslo, Norway.
Dajiang QinGuangdong Engineering Technology Research Center of Biological Targeting Diagnosis, Therapy and Rehabilitation, The Fifth Affiliated Hospital, Guangzhou Medical University, No.621 Gangwan Road, Guangzhou, China; Centre for Regenerative Medicine and Health, Hong Kong Institute of Science & Innovation, Chinese Academy of Sciences, Hong Kong, China. Electronic address: qin_dajiang@gzhmu.edu.cn.
Huanxing SuState Key Laboratory of Mechanism and Quality of Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China. Electronic address: huanxingsu@um.edu.mo.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lysosomal dysfunction is a core pathological driver of neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS). Transcription factor EB (TFEB) serves as a master regulator of lysosomal biogenesis, and its pharmacological activation represents a strategy to restore lysosomal function in disease and aging. Here, using a series of artificial intelligence-powered computational virtual screening workflows, we have identified isoginkgetin (ISO), a small-molecule compound, as a potent TFEB activator that promotes mechanistic target of rapamycin complex 1 (mTORC1)-independent TFEB nuclear translocation to enhance lysosomal biogenesis and function. Mechanistically, ISO functions as an ATP-competitive inhibitor that binds to the key Lys85 residue within the ATP-binding pocket of glycogen synthase kinase 3β (GSK-3β), thereby regulating the GSK-3β-TFEB signaling axis to activate TFEB nuclear translocation. Functionally, ISO improves lysosomal function and protects motor neurons differentiated from induced pluripotent stem cells derived from patients with ALS from degeneration. Collectively, these results support the hypothesis that lysosomal dysfunction is a druggable target for ALS.

Indexed as

Amyotrophic Lateral SclerosisBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsGlycogen Synthase Kinase 3 betaMotor NeuronsNeuroprotective AgentsAnimalsHumansInduced Pluripotent Stem CellsLysosomesMiceSignal TransductionBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsGlycogen Synthase Kinase 3 betaNeuroprotective AgentsTFEB protein, humanAmyotrophic lateral sclerosisArtificial intelligenceGSK-3β–TFEB axisIsoginkgetinLysosome

Identifiers

PMID41912102
PMCPMC13132972

What OpenQuestion holds

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Registered trials

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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.