Evidence map›Paper›PMID 34071003›Full record

ArticleInternational journal of molecular sciences2021

Reduction of Superoxide Dismutase 1 Delays Regeneration of Cardiotoxin-Injured Skeletal Muscle in KK/Ta-

Yuya Takahashi, Tatsunori Shimizu, Shunsuke Kato, Mitsuhiko Nara, Yumi Suganuma, Takehiro Sato, Tsukasa Morii, Yuichiro Yamada, Hiroki Fujita

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Oxidative Stress and Skeletal Muscle Function.International journal of molecular sciences · 2023
    Article
  8. Review
  9. Skeletal Muscle Regeneration in Cardiotoxin-Induced Muscle Injury Models.International journal of molecular sciences · 2022
    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 1 institution in 1 country.

Yuya TakahashiDepartment of Metabolism and Endocrinology, Akita University Graduate School of Medicine, 1-1-1 Hondo, Akita 010-8543, Japan.
Tatsunori ShimizuDepartment of Metabolism and Endocrinology, Akita University Graduate School of Medicine, 1-1-1 Hondo, Akita 010-8543, Japan.
Shunsuke KatoDepartment of Metabolism and Endocrinology, Akita University Graduate School of Medicine, 1-1-1 Hondo, Akita 010-8543, Japan.
Mitsuhiko NaraDepartment of Metabolism and Endocrinology, Akita University Graduate School of Medicine, 1-1-1 Hondo, Akita 010-8543, Japan.ORCID 0000-0002-7844-8564
Yumi SuganumaDepartment of Metabolism and Endocrinology, Akita University Graduate School of Medicine, 1-1-1 Hondo, Akita 010-8543, Japan.
Takehiro SatoDepartment of Metabolism and Endocrinology, Akita University Graduate School of Medicine, 1-1-1 Hondo, Akita 010-8543, Japan.
Tsukasa MoriiDepartment of Metabolism and Endocrinology, Akita University Graduate School of Medicine, 1-1-1 Hondo, Akita 010-8543, Japan.
Yuichiro YamadaDepartment of Metabolism and Endocrinology, Akita University Graduate School of Medicine, 1-1-1 Hondo, Akita 010-8543, Japan.
Hiroki FujitaDepartment of Metabolism and Endocrinology, Akita University Graduate School of Medicine, 1-1-1 Hondo, Akita 010-8543, Japan.
Akita University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Superoxide dismutase (SOD) is a major antioxidant enzyme for superoxide removal, and cytoplasmic SOD (SOD1) is expressed as a predominant isoform in all cells. We previously reported that renal SOD1 deficiency accelerates the progression of diabetic nephropathy (DN) via increasing renal oxidative stress. To evaluate whether the degree of SOD1 expression determines regeneration capacity and sarcopenic phenotypes of skeletal muscles under incipient and advanced DN conditions, we investigated the alterations of SOD1 expression, oxidative stress marker, inflammation, fibrosis, and regeneration capacity in cardiotoxin (CTX)-injured tibialis anterior (TA) muscles of two Akita diabetic mouse models with different susceptibility to DN, DN-resistant C57BL/6-

Indexed as

AnimalsCardiotoxinsCollagen Type ICollagen Type I, alpha 1 ChainDiabetes Mellitus, ExperimentalDiabetic NephropathiesDisease ProgressionEnzyme InductionFibrosisGene Expression Regulation, EnzymologicGenetic Predisposition to DiseaseGlomerular MesangiumInflammationInsulinMaleMiceCardiotoxinsCollagen Type ICollagen Type I, alpha 1 ChainIns2 protein, mouseInsulinSod1 protein, mouseSuperoxide Dismutase-1Superoxidesakita mousecardiotoxin injurydiabetic nephropathymuscle regenerationoxidative stresssuperoxide dismutase 1

Identifiers

PMID34071003
PMCPMC8197123
OpenAlexW3164259343

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.