Evidence map›Paper›PMID 33136552›Full record

ArticleAging2020

High phosphate induces skeletal muscle atrophy and suppresses myogenic differentiation by increasing oxidative stress and activating Nrf2 signaling.

Lin-Huei Chung, Shu-Ting Liu, Shih-Ming Huang, Donald M Salter, Herng-Sheng Lee, Yu-Juei Hsu

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Hyperphosphatemia Contributes to Skeletal Muscle Atrophy in Mice.International journal of molecular sciences · 2024
    Article
  10. A role for sirtuin 1 in FGF23 activation following β-glycerophosphate treatment.Pflugers Archiv : European journal of physiology · 2024
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Phosphate Burden and Organ Dysfunction.Frontiers in aging · 2022
    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 4 institutions in 2 countries.

Lin-Huei ChungGraduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan.
Shu-Ting LiuDepartment of Biochemistry, National Defense Medical Center, Taipei, Taiwan.
Shih-Ming HuangGraduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan.
Donald M SalterCentre for Genomic and Experimental Medicine, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, UK.
Herng-Sheng LeeDepartment of Pathology and Laboratory Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan.
Yu-Juei HsuGraduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan.
National Defense Medical Center · TWKaohsiung Veterans General Hospital · TWTri-Service General Hospital · TWUniversity of Edinburgh · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skeletal muscle wasting represents both a common phenotype of aging and a feature of pathological conditions such as chronic kidney disease (CKD). Although both clinical data and genetic experiments in mice suggest that hyperphosphatemia accelerates muscle wasting, the underlying mechanism remains unclear. Here, we showed that inorganic phosphate (Pi) dose-dependently decreases myotube size, fusion index, and myogenin expression in mouse C2C12 skeletal muscle cells. These changes were accompanied by increases in reactive oxygen species (ROS) production and Nrf2 and p62 expression, and reductions in mitochondrial membrane potential (MMP) and Keap1 expression. Inhibition of Pi entry, cytosolic ROS production, or Nrf2 activation reversed the effects of high Pi on Nrf2, p62, and myogenin expression. Overexpression of Nrf2 respectively increased and decreased the promoter activity of

Indexed as

Cell DifferentiationMuscle DevelopmentOxidative StressAnimalsCell LineDisease Models, AnimalHyperphosphatemiaKelch-Like ECH-Associated Protein 1MaleMiceMice, Inbred C57BLMuscular AtrophyMyoblasts, SkeletalMyogeninNF-E2-Related Factor 2PhosphatesKeap1 protein, mouseKelch-Like ECH-Associated Protein 1MyogeninMyog protein, mouseNfe2l2 protein, mouseNF-E2-Related Factor 2PhosphatesSequestosome-1 Proteinsodium phosphateSqstm1 protein, mousehyperphosphatemiamuscle wastingmyogenic differentiationNrf2oxidative stress

Identifiers

PMID33136552
PMCPMC7695395
OpenAlexW3095821485

What OpenQuestion holds

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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.