Evidence map›Paper›PMID 34461564›Full record

ReviewCurrent opinion in pharmacology2021

Pharmacologic approaches to prevent skeletal muscle atrophy after spinal cord injury.

Dana M Otzel, Hui Jean Kok, Zachary A Graham, Elisabeth R Barton, Joshua F Yarrow

Open access · hybridAbstract readReview
In one paragraph

Review in Current opinion in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.8field-weighted citation impact, top 14% of its field
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

28 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
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  7. Electrical Stimulation Therapy - Dedicated to the Perfect Plastic Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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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

5 authors at 3 institutions in 1 country.

Dana M OtzelBrain Rehabilitation Research Center, Malcom Randall Department of Veterans Affairs Medical Center, North Florida/South Georgia Veterans Health System, Gainesville, FL, USA.
Hui Jean KokDepartment of Applied Physiology & Kinesiology, College of Health & Human Performance, University of Florida, Gainesville, FL, USA.
Zachary A GrahamResearch Service, Birmingham VA Medical Center, Birmingham, AL, USA; Department of Cell, Development and Integrative Biology, University of Alabama-Birmingham, Birmingham, AL, USA.
Elisabeth R BartonDepartment of Applied Physiology & Kinesiology, College of Health & Human Performance, University of Florida, Gainesville, FL, USA.
Joshua F YarrowBrain Rehabilitation Research Center, Malcom Randall Department of Veterans Affairs Medical Center, North Florida/South Georgia Veterans Health System, Gainesville, FL, USA; Research Service, Malcom Randall Department of Veterans Affairs Medical Center, North Florida/South Georgia Veterans Health System, Gainesville, FL, USA; Division of Endocrinology, Diabetes, and Metabolism, University of Florida College of Medicine, Gainesville, FL, USA. Electronic address: Joshua.Yarrow@medicine.ufl.edu.
University of Florida · USNorth Florida/South Georgia Veterans Health System · USUniversity of Alabama at Birmingham · US

Funding

Mechanisms and treatments of mitochondrial dysfunction in paralyzed skeletal muscle after spinal cord injuryIK2RX002781 · VA · JAMES J PETERS VA MEDICAL CENTER · PI GRAHAM, ZACHARY AARON · 2018 to 2024
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RRD VA I01 RX002447RRD VA IK2 RX002781
6 · The paper itself

Abstract

Skeletal muscle atrophy is a hallmark of severe spinal cord injury (SCI) that is precipitated by the neural insult and paralysis. Additionally, other factors may influence muscle loss, including systemic inflammation, low testosterone, low insulin-like growth factor (IGF)-1, and high-dose glucocorticoid treatment. The signaling cascades that drive SCI-induced muscle loss are common among most forms of disuse atrophy and include ubiquitin-proteasome signaling and others. However, differing magnitudes and patterns of atrophic signals exist after SCI versus other disuse conditions and are accompanied by endogenous inhibition of IGF-1/PI3K/Akt signaling, which combine to produce exceedingly rapid atrophy. Several well-established anabolic agents, including androgens and myostatin inhibitors, display diminished ability to prevent SCI-induced atrophy, while ursolic acid and β2-agonists more effectively attenuate muscle loss. Strategies combining physical rehabilitation regimens to reload the paralyzed limbs with drugs targeting the underlying molecular pathways hold the greatest potential to improve muscle recovery after severe SCI.

Indexed as

Pharmaceutical PreparationsSpinal Cord InjuriesHumansMuscle, SkeletalMuscular AtrophyPharmaceutical PreparationsActeosideActivin IIb receptorActivity-based physical therapyAnabolicAndrogenAntioxidantAtrogin-1AtrophyBeta 2 agonistBodyweight-supported treadmill trainingClenbuterolDenervationDisuseElamipretideEpicatechinFormoterolFOXOFunctional electrical stimulationHypertrophyIgf-1Insulin-like growth factor 1MAFbxmTORMuRF1MuscleMusculoskeletalMyostatinNeuromuscular electrical stimulationParalysisParalyzedSpinal cord injurySS-31TestosteroneTestosterone replacement therapyTGF betaTransforming growth factor betaUbiquitinUnloadingUrsolic acidVerbascoside

Identifiers

PMID34461564
PMCPMC9190029
OpenAlexW3197468344

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.