Evidence map›Paper›PMID 40848171›Full record

ArticleNeuroscience bulletin2026

HSF-1 Regulates Autophagy to Govern Motor Function and Facilitate Toxic Protein Clearance in a C. elegans Model of Amyotrophic Lateral Sclerosis.

Hui Xu, Yaping Shao, Jun Zhang, Yang Ni, Guowang Xu, Cong Liu, Yi Liang, Weidong Le

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuroscience bulletin, 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. 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

8 authors.

Hui XuKey Laboratory of Liaoning Province for Research on the Pathogenic Mechanisms of Neurological Diseases, The First Affiliated Hospital of Dalian Medical University, Dalian, 116021, China. xuhui@dmu.edu.cn.ORCID http://orcid.org/0000-0001-5516-2814
Yaping ShaoKey Laboratory of Liaoning Province for Research on the Pathogenic Mechanisms of Neurological Diseases, The First Affiliated Hospital of Dalian Medical University, Dalian, 116021, China.
Jun ZhangKey Laboratory of Liaoning Province for Research on the Pathogenic Mechanisms of Neurological Diseases, The First Affiliated Hospital of Dalian Medical University, Dalian, 116021, China.
Yang NiKey Laboratory of Liaoning Province for Research on the Pathogenic Mechanisms of Neurological Diseases, The First Affiliated Hospital of Dalian Medical University, Dalian, 116021, China.
Guowang XuCAS Key Laboratory of Separation Science for Analytical Chemistry, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian, 116023, China.
Cong LiuInterdisciplinary Research Center on Biology and Chemistry, State Key Laboratory of Chemical Biology, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai, 200032, China.
Yi LiangHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, TaiKang Center for Life and Medical Sciences, Wuhan University, Wuhan, 430072, China.
Weidong LeKey Laboratory of Liaoning Province for Research on the Pathogenic Mechanisms of Neurological Diseases, The First Affiliated Hospital of Dalian Medical University, Dalian, 116021, China. wdle@sibs.ac.cn.ORCID http://orcid.org/0000-0001-7459-2705

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heat shock factor-1 (HSF-1) plays a crucial role in orchestrating stress responses across diverse organisms and disease conditions. Here, we investigate how the HSF-1 signaling pathway influences the degradation of toxic proteins and neuropathological changes in the Caenorhabditis elegans model of amyotrophic lateral sclerosis (ALS). We found that overexpressing HSF-1 improves locomotor ability and increases the survival rate of ALS C. elegans. Moreover, we observed a deceleration of motor neuron degeneration, demonstrating the protective effect of HSF-1 on neurodegenerative processes. Transcriptomic analysis revealed notable changes in genes associated with autophagy and neurodegeneration, underscoring HSF-1's critical involvement in ALS pathology. In addition, metabolomic profiling further highlighted the involvement of this pathway in metabolic reprogramming. Overall, our study underscores the critical role of the HSF-1 signaling pathway in improving survival rate, movement velocity, cellular integrity, and metabolic adaptation, providing new insights into the mechanisms underlying ALS and potential targets for therapeutic intervention.

Indexed as

Amyotrophic Lateral SclerosisAutophagyCaenorhabditis elegans ProteinsTranscription FactorsAnimalsAnimals, Genetically ModifiedCaenorhabditis elegansDisease Models, AnimalLocomotionMotor NeuronsSignal TransductionCaenorhabditis elegans Proteinsheat shock factor-1, C elegansTranscription FactorsALSAutophagyCaenorhabditis elegansHSF-1 signaling pathwayNeuroprotection

Identifiers

PMID40848171
PMCPMC13031479

What OpenQuestion 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 OpenQuestion graph.