Evidence map›Paper›PMID 39314333›Full record

ArticlebioRxiv : the preprint server for biology2024

The myokine FGF21 associates with enhanced survival in ALS and mitigates stress-induced cytotoxicity.

Abhishek Guha, Ying Si, Reed Smith, Mohamed Kazamel, Nan Jiang, Katherine A Smith, Anna Thalacker-Mercer, Brijesh K Singh, Ritchie Ho, Shaida A Andrabi and 5 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. 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

5 · Who and what money

Authors and funding

15 authors.

Abhishek GuhaDepartment of Neurology, University of Alabama at Birmingham, Birmingham, AL 35294.ORCID 0000-0003-2767-9941
Ying SiDepartment of Neurology, University of Alabama at Birmingham, Birmingham, AL 35294.
Reed SmithDepartment of Neurology, University of Alabama at Birmingham, Birmingham, AL 35294.
Mohamed KazamelDepartment of Neurology, University of Alabama at Birmingham, Birmingham, AL 35294.
Nan JiangDepartment of Neurology, University of Alabama at Birmingham, Birmingham, AL 35294.
Katherine A SmithDepartment of Neurology, University of Alabama at Birmingham, Birmingham, AL 35294.
Anna Thalacker-MercerBirmingham Veterans Affairs Medical Center, Birmingham, AL 35294.ORCID 0000-0002-9124-7927
Brijesh K SinghBoard of Governors Regenerative Medicine Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Ritchie HoBoard of Governors Regenerative Medicine Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.ORCID 0000-0003-1496-4436
Shaida A AndrabiDepartment of Neurology, University of Alabama at Birmingham, Birmingham, AL 35294.
Joao D Tavares Da Silva PereiraDepartment of Neurology, University of Alabama at Birmingham, Birmingham, AL 35294.
Juliana S SalgadoDepartment of Neuroscience, Yale University School of Medicine, New Haven, CT 06510, USA.
Manasi AgrawalDepartment of Neuroscience, Yale University School of Medicine, New Haven, CT 06510, USA.
Emina Horvat VelicDepartment of Neuroscience, Yale University School of Medicine, New Haven, CT 06510, USA.
Peter H KingDepartment of Neurology, University of Alabama at Birmingham, Birmingham, AL 35294.ORCID 0000-0001-9391-7464

Funding

Smad Signaling in Skeletal Muscle as a Biomarker of Disease Progression in ALSR01NS092651 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI KING, PETER H · 2016 to 2020
$1.6M
FGF23: a novel biomarker in ALS and moreR21NS111275 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI KING, PETER H · 2019 to 2019
$422k
VA Biorepository Brain BankI01BX002466 · VA · VA BOSTON HEALTH CARE SYSTEM · PI Ann C. McKee, Haining Zhu · 2014 to 2026
–
Sustained Smad signaling in ALS muscle promotes disease progression through a dysregulated miRNA transcriptomeI01BX006231 · VA · BIRMINGHAM VA MEDICAL CENTER · PI KING, PETER H · 2024 to 2025
–
BLRD VA I01 BX002466BLRD VA I01 BX006231NINDS NIH HHS R01 NS092651NINDS NIH HHS R21 NS111275
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is an age-related and fatal neurodegenerative disease characterized by progressive muscle weakness. There is marked heterogeneity in clinical presentation, progression, and pathophysiology with only modest treatments to slow disease progression. Molecular markers that provide insight into this heterogeneity are crucial for clinical management and identification of new therapeutic targets. In a prior muscle miRNA sequencing investigation, we identified altered FGF pathways in ALS muscle, leading us to investigate FGF21. We analyzed human ALS muscle biopsy samples and found a large increase in FGF21 expression with localization to atrophic myofibers and surrounding endomysium. A concomitant increase in FGF21 was detected in ALS spinal cords which correlated with muscle levels. FGF21 was increased in the SOD1

Indexed as

ALS biomarkerFibroblast growth factor 21human skeletal musclemotor neuronsoxidative stress responseβ-Klotho

Identifiers

PMID39314333
PMCPMC11419072

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.