Evidence map›Paper›PMID 35163674›Full record

ArticleInternational journal of molecular sciences2022

Gene Transfer of Skeletal Muscle-Type Myosin Light Chain Kinase via Adeno-Associated Virus 6 Improves Muscle Functions in an Amyotrophic Lateral Sclerosis Mouse Model.

Ryohei Oya, Osamu Tsukamoto, Tatsuro Hitsumoto, Naoya Nakahara, Chisato Okamoto, Ken Matsuoka, Hisakazu Kato, Hidenori Inohara, Seiji Takashima

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. 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
0.4field-weighted citation impact, top 41% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Skeletal muscle dysfunction in amyotrophic lateral sclerosis: a mitochondrial perspective and therapeutic approaches.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
    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

9 authors at 2 institutions in 1 country.

Ryohei OyaDepartment of Medical Biochemistry, Osaka University Graduate School of Medicine/Frontier Biosciences, Osaka 565-0871, Japan.ORCID 0000-0001-8991-0315
Osamu TsukamotoDepartment of Medical Biochemistry, Osaka University Graduate School of Medicine/Frontier Biosciences, Osaka 565-0871, Japan.
Tatsuro HitsumotoDepartment of Medical Biochemistry, Osaka University Graduate School of Medicine/Frontier Biosciences, Osaka 565-0871, Japan.
Naoya NakaharaDepartment of Molecular Physiology, The Jikei University School of Medicine, Tokyo 105-8461, Japan.
Chisato OkamotoDepartment of Medical Biochemistry, Osaka University Graduate School of Medicine/Frontier Biosciences, Osaka 565-0871, Japan.ORCID 0000-0002-0671-793X
Ken MatsuokaDepartment of Medical Biochemistry, Osaka University Graduate School of Medicine/Frontier Biosciences, Osaka 565-0871, Japan.
Hisakazu KatoDepartment of Medical Biochemistry, Osaka University Graduate School of Medicine/Frontier Biosciences, Osaka 565-0871, Japan.ORCID 0000-0003-4619-3680
Hidenori InoharaDepartment of Otorhinolaryngology Head and Neck Surgery, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan.
Seiji TakashimaDepartment of Medical Biochemistry, Osaka University Graduate School of Medicine/Frontier Biosciences, Osaka 565-0871, Japan.
The University of Osaka · JPJikei University School of Medicine · JP

Funding

Japan Society for the Promotion of Science 17K09578, 18K15366
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that shows progressive muscle weakness. A few treatments exist including symptomatic therapies, which can prolong survival or reduce a symptom; however, no fundamental therapies have been found. As a therapeutic strategy, enhancing muscle force is important for patients' quality of life. In this study, we focused on skeletal muscle-specific myosin regulatory light chain kinase (skMLCK), which potentially enhances muscle contraction, as overexpression of skMLCK was thought to improve muscle function. The adeno-associated virus serotype 6 encoding skMLCK (AAV6/skMLCK) and eGFP (control) was produced and injected intramuscularly into the lower limbs of SOD1

Indexed as

Gene Transfer TechniquesAmyotrophic Lateral SclerosisAnimalsBiomechanical PhenomenaDependovirusDisease Models, AnimalGenetic VectorsHEK293 CellsHumansInjections, IntramuscularMiceMice, Inbred C57BLMuscle, SkeletalMyosin-Light-Chain KinaseTetanyMyosin-Light-Chain Kinaseadeno-associated virus 6amyotrophic lateral sclerosisgene therapymuscle functionmyosin light chain kinase

Identifiers

PMID35163674
PMCPMC8836241
OpenAlexW4210534167

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.