Evidence map›Paper›PMID 39769213›Full record

ArticleInternational journal of molecular sciences2024

Chronic Oxidative Stress and Stress Granule Formation in UBQLN2 ALS Neurons: Insights into Neuronal Degeneration and Potential Therapeutic Targets.

Ao Gu, Yiti Zhang, Jianfeng He, Mingri Zhao, Lingjie Ding, Wanxi Liu, Jianing Xiao, Jiali Huang, Mujun Liu, Xionghao Liu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Optimized Preparation ofCurrent issues in molecular biology · 2026
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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

10 authors.

Ao GuMOE Key Lab of Rare Pediatric Diseases & Hunan Key Laboratory of Medical Genetics of the School of Life Sciences, Central South University, Changsha 410017, China.
Yiti ZhangMOE Key Lab of Rare Pediatric Diseases & Hunan Key Laboratory of Medical Genetics of the School of Life Sciences, Central South University, Changsha 410017, China.ORCID 0000-0002-4245-2879
Jianfeng HeMOE Key Lab of Rare Pediatric Diseases & Hunan Key Laboratory of Medical Genetics of the School of Life Sciences, Central South University, Changsha 410017, China.
Mingri ZhaoMOE Key Lab of Rare Pediatric Diseases & Hunan Key Laboratory of Medical Genetics of the School of Life Sciences, Central South University, Changsha 410017, China.ORCID 0000-0002-8260-7935
Lingjie DingMOE Key Lab of Rare Pediatric Diseases & Hunan Key Laboratory of Medical Genetics of the School of Life Sciences, Central South University, Changsha 410017, China.
Wanxi LiuMOE Key Lab of Rare Pediatric Diseases & Hunan Key Laboratory of Medical Genetics of the School of Life Sciences, Central South University, Changsha 410017, China.
Jianing XiaoMOE Key Lab of Rare Pediatric Diseases & Hunan Key Laboratory of Medical Genetics of the School of Life Sciences, Central South University, Changsha 410017, China.
Jiali HuangMOE Key Lab of Rare Pediatric Diseases & Hunan Key Laboratory of Medical Genetics of the School of Life Sciences, Central South University, Changsha 410017, China.
Mujun LiuDepartment of Cell Biology, School of Life Sciences, Central South University, Changsha 410017, China.ORCID 0000-0002-1558-1448
Xionghao LiuMOE Key Lab of Rare Pediatric Diseases & Hunan Key Laboratory of Medical Genetics of the School of Life Sciences, Central South University, Changsha 410017, China.ORCID 0000-0002-2633-7096

Funding

Fundamental Research Funds for the Central Universities of Central South University 1053320222758National Key Research and Development Program of China 2016YFC0905100Natural Science Foundation of Changsha, China kq2202077Natural Science Foundation of Hunan Province, China 2021JJ30801
6 · The paper itself

Abstract

The pathogenesis of neurodegenerative diseases results from the interplay between genetic and environmental factors. Aging and chronic oxidative stress are critical contributors to neurodegeneration. UBQLN2, a ubiquitin-related protein, aids in protein degradation and protects against oxidative stress. In ALS neurons harboring UBQLN2 mutations, oxidative stress accelerates pathological changes, yet the precise mechanisms remain unclear. Using induced motor neurons (iMNs) derived from UBQLN2 P497H iPSCs, we observed ALS-like phenotypes, including TDP-43 mislocalization, increased cell death, and reduced viability. Sodium arsenite (SA)-induced oxidative stress triggered stress granule formation, while autophagy dysfunction exacerbated neuronal degeneration. CHX and bosutinib treatments reduced ubiquitinated protein accumulation and alleviated degeneration, highlighting potential therapeutic pathways. These findings emphasize the role of chronic oxidative stress and stress granule formation in UBQLN2 ALS, offering insights into novel therapeutic targets.

Indexed as

Amyotrophic Lateral SclerosisAutophagy-Related ProteinsMotor NeuronsOxidative StressAdaptor Proteins, Signal TransducingAutophagyCell Cycle ProteinsDNA-Binding ProteinsHumansInduced Pluripotent Stem CellsNerve DegenerationSodium CompoundsStress GranulesAdaptor Proteins, Signal TransducingAutophagy-Related ProteinsCell Cycle ProteinsDNA-Binding ProteinsSodium CompoundsUBQLN2 protein, humanALSmotor neuronsneurodegenerative diseasesoxidative stressstress granuleUBQLN2

Identifiers

PMID39769213
PMCPMC11678478

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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.