Evidence map›Paper›PMID 35144051›Full record

ArticleRedox biology2022

Selenoprotein K protects skeletal muscle from damage and is required for satellite cells-mediated myogenic differentiation.

Shengchen Wang, Xia Zhao, Qingqing Liu, Yue Wang, Shu Li, Shiwen Xu

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2022. 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
8.3field-weighted citation impact, top 1% 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, 77 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Selenoprotein K at the intersection of cellular pathways.Archives of biochemistry and biophysics · 2025
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Se Alleviated Pb-Caused Neurotoxicity in Chickens:Antioxidants (Basel, Switzerland) · 2024
    Article
  18. Article
  19. Article
  20. Article
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

6 authors at 1 institution in 1 country.

Shengchen WangCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR China.
Xia ZhaoCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR China.
Qingqing LiuCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR China.
Yue WangCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR China.
Shu LiCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR China. Electronic address: lishu@neau.edu.cn.
Shiwen XuCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR China; Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR China. Electronic address: shiwenxu@neau.edu.cn.
Northeast Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The regeneration of adult skeletal muscle after injury is primarily initiated by satellite cells (SCs), but the regulatory mechanisms of cells committed to myogenic differentiation remain poorly explored. Small molecular selenoprotein K (SelK) plays crucial roles in the modulation of endoplasmic reticulum (ER) stress and against oxidative stress. Here, we first showed that SelK expression is activated in myogenic cells during differentiation both in vivo and in vitro. Meanwhile, loss of SelK delayed skeletal muscle regeneration, inhibited the development of myoblasts into myotubes, and was accompanied by reduced expression of myogenic regulatory factors (MRFs). Moreover, ER stress, intracellular reactive oxygen species (ROS), autophagy and apoptosis under myogenesis induction were more severe in SelK-deficient mice and cells than in the corresponding control groups. Supplementation with specific inhibitors to alleviate excessive ER stress or oxidative stress partly rescued the differentiation potential and formation of myotubes. Notably, we demonstrated that Self-mediated regulation of cellular redox status was primarily derived from its subsequent effects on ER stress. Together, our results suggest that SelK protects skeletal muscle from damage and is a crucial regulator of myogenesis.

Indexed as

Muscle DevelopmentMyoblastsSelenoproteinsAnimalsCell DifferentiationMiceMuscle Fibers, SkeletalMuscle, Skeletalselenoprotein K, mouseSelenoproteinsEndoplasmic reticulum stressMyogenesisOxidative stressSatellite cellsSelenoprotein KSkeletal muscle

Identifiers

PMID35144051
PMCPMC8844831
OpenAlexW4210804371

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.