Evidence map›Paper›PMID 41750323›Full record

ArticleBiomolecules2026

Absence of Neuromuscular Dysfunction in Mice with Gut Epithelium-Restricted Expression of ALS Mutation hSOD1

Li Dong, Xuejun Li, Ang Li, Jianxun Yi, Yanan Vockery, Yan Chang, Zui Pan, Marco Brotto, Jingsong Zhou

Abstract read
In one paragraph

Article in Biomolecules, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Li DongDepartment of Kinesiology, College of Nursing and Health Innovation, University of Texas at Arlington, Arlington, TX 76019, USA.ORCID 0009-0005-1574-068X
Xuejun LiDepartment of Kinesiology, College of Nursing and Health Innovation, University of Texas at Arlington, Arlington, TX 76019, USA.
Ang LiDepartment of Kinesiology, College of Nursing and Health Innovation, University of Texas at Arlington, Arlington, TX 76019, USA.ORCID 0000-0002-8784-4702
Jianxun YiDepartment of Kinesiology, College of Nursing and Health Innovation, University of Texas at Arlington, Arlington, TX 76019, USA.
Yanan VockeryDepartment of Kinesiology, College of Nursing and Health Innovation, University of Texas at Arlington, Arlington, TX 76019, USA.
Yan ChangBone-Muscle Research Center, College of Nursing and Health Innovation, University of Texas at Arlington, Arlington, TX 76010, USA.
Zui PanBone-Muscle Research Center, College of Nursing and Health Innovation, University of Texas at Arlington, Arlington, TX 76010, USA.ORCID 0000-0003-4105-901X
Marco BrottoBone-Muscle Research Center, College of Nursing and Health Innovation, University of Texas at Arlington, Arlington, TX 76010, USA.
Jingsong ZhouDepartment of Kinesiology, College of Nursing and Health Innovation, University of Texas at Arlington, Arlington, TX 76019, USA.

Funding

Preserving Mitochondrial Function for Alleviating ALS ProgressionR01NS105621 · NINDS · UNIVERSITY OF TEXAS ARLINGTON · PI BROTTO, MARCO, ZHOU, JINGSONG · 2019 to 2023
$2.9M
Ca signaling cross-talk from SR to mitochondria in heart muscleR01HL138570 · NHLBI · OHIO STATE UNIVERSITY · PI LIN, PEI-HUI, ZHOU, JINGSONG · 2018 to 2021
$2.6M
Multifaceted role of MG53 in alleviating neuromuscular function decline in ALSR01NS129219 · NINDS · UNIVERSITY OF TEXAS ARLINGTON · PI Jianjie Ma, Lyle Wilfred Ostrow · 2023 to 2026
$2.5M
Ca Signaling in Progression of Amyotrophic Lateral Sclerosis in Skeletal MuscleR01AR057404 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI ZHOU, JINGSONG · 2010 to 2014
$1.6M
Bank of America 16-IIP-288National Institute of Health R01HL138570National Institute of Health R01NS105621NHLBI NIH HHS R01 HL138570NIAMS NIH HHS R01 AR057404NINDS NIH HHS R01 NS105621NINDS NIH HHS R01 NS129219United States Department of Defense AL170061(W81XWH1810684)
6 · The paper itself

Abstract

Amyotrophic Lateral Sclerosis (ALS) is a devastating neuromuscular disorder characterized by the progressive loss of motor neurons and skeletal muscle, ultimately leading to respiratory failure and death, typically within 3-5 years following diagnosis. While the death of motor neurons is the pathological hallmark, ALS is increasingly recognized as a systemic disorder involving non-motor systems. Gastrointestinal dysfunction has been widely observed in both ALS patients and animal models. However, because gut abnormalities and neuromuscular degeneration are intertwined during ALS disease progression, it remains unclear whether these gut abnormalities are merely a consequence of neuromuscular degeneration or whether they play a crucial role in initiating it. In this study, we investigated whether an ALS-associated mutation expressed exclusively in the gut can directly affect neuromuscular function. We generated a novel transgenic mouse model, Gut-hG93A, which overexpresses the human ALS mutation hSOD1

Indexed as

Amyotrophic Lateral SclerosisIntestinal MucosaMutationSuperoxide Dismutase-1AnimalsDisease Models, AnimalHumansIntestinal Barrier FunctionMiceMice, TransgenicMuscle, SkeletalSOD1 protein, humanSuperoxide Dismutase-1amyotrophic lateral sclerosis (ALS)Cre-Loxgut epitheliumhuman ALS mutation hSOD1G93Aintestinal permeabilitymuscle contractilityskeletal muscletransgenic mouse

Identifiers

PMID41750323
PMCPMC12938467

What Socratic holds

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LicenceCC BY
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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.