Evidence map›Paper›PMID 33722298›Full record

ArticleSkeletal muscle2021

MiR-1290 promotes myoblast differentiation and protects against myotube atrophy via Akt/p70/FoxO3 pathway regulation.

Ji Che, Cuidi Xu, Yuanyuan Wu, Peiyu Jia, Qi Han, Yantao Ma, Xiaolei Wang, Yongjun Zheng

Open access · goldAbstract read
In one paragraph

Article in Skeletal muscle, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Journal of microbiology and biotechnology · 2026
    Article
  3. Review
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  6. Review
  7. Epigenetics of Skeletal Muscle Atrophy.International journal of molecular sciences · 2024
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. An Insight into miR-1290: An Oncogenic miRNA with Diagnostic Potential.International journal of molecular sciences · 2022
    Review
  17. 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

8 authors at 2 institutions in 1 country.

Ji Che *Department of Pain, Huadong Hospital, Shanghai Key Laboratory of Clinical Geriatric Medicine, Fudan University, No. 221, West YanAn Rd, Shanghai, 200040, P.R. China.
Cuidi Xu *Department of Osteoporosis and Bone Disease, Huadong Hospital, Research Section of Geriatric Metabolic Bone Disease, Shanghai Geriatric Institute, Shanghai, China.
Yuanyuan WuDepartment of Pain, Huadong Hospital, Shanghai Key Laboratory of Clinical Geriatric Medicine, Fudan University, No. 221, West YanAn Rd, Shanghai, 200040, P.R. China.
Peiyu JiaDepartment of Pain, Huadong Hospital, Shanghai Key Laboratory of Clinical Geriatric Medicine, Fudan University, No. 221, West YanAn Rd, Shanghai, 200040, P.R. China.
Qi HanDepartment of Pain, Huadong Hospital, Shanghai Key Laboratory of Clinical Geriatric Medicine, Fudan University, No. 221, West YanAn Rd, Shanghai, 200040, P.R. China.
Yantao MaDepartment of Pain, Huadong Hospital, Shanghai Key Laboratory of Clinical Geriatric Medicine, Fudan University, No. 221, West YanAn Rd, Shanghai, 200040, P.R. China.
Xiaolei WangDepartment of Pain, Huadong Hospital, Shanghai Key Laboratory of Clinical Geriatric Medicine, Fudan University, No. 221, West YanAn Rd, Shanghai, 200040, P.R. China. 200100798@163.com.
Yongjun ZhengDepartment of Pain, Huadong Hospital, Shanghai Key Laboratory of Clinical Geriatric Medicine, Fudan University, No. 221, West YanAn Rd, Shanghai, 200040, P.R. China. zhengyongjun@fudan.edu.cn.
Huadong Hospital · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSarcopenia is a common skeletal disease related to myogenic disorders and muscle atrophy. Current clinical management has limited effectiveness. We sought to investigate the role of miR-1290 in myoblast differentiation and muscle atrophy.

methodsBy transfecting miR-1290 into C2C12 cells, we investigated whether miR-1290 regulates myogenesis and myotube atrophy via AKT/P70 signaling pathway. MHC staining was performed to assess myoblast differentiation. Differentiation-related MHC, Myod, and Myog protein levels, and atrophy-related MuRF1 and atrogin-1 were explored by western blot. An LPS-induced muscle atrophy rat model was developed. RT-PCR was conducted to analyze miR-1290 serum levels in muscle atrophy patients and normal controls (NCs).

resultsThe miR-1290 transfection increased MHC-positive cells and MHC, Myod, and Myog protein levels in the miR-1290 transfection group, demonstrating that miR-1290 promoted C2C12 myoblast differentiation. Myotube diameter in the miR-1290 transfection group was higher than in the TNF-α-induced model group. Western blot analysis showed decreased MuRF1 and atrogin-1 levels in the miR-1290 transfection group compared with the model group, demonstrating that miR-1290 protected against myoblast cellular atrophy. Luciferase assay and western blot analysis showed that miR-1290 regulation was likely caused by AKT/p70/FOXO3 phosphorylation activation. In the LPS-induced muscle atrophy rat model, miR-1290 mimics ameliorated gastrocnemius muscle loss and increased muscle fiber cross-sectional area. Clinically, miR-1290 serum level was significantly decreased in muscle atrophy patients.

conclusionsWe found that miR-1290 enhances myoblast differentiation and inhibits myotube atrophy through Akt/p70/FoxO3 signaling in vitro and in vivo. In addition, miR-1290 may be a potential therapeutic target for sarcopenia treatment.

Indexed as

MicroRNAsMuscular AtrophyAnimalsCell DifferentiationCell LineForkhead Box Protein O3HumansMuscle Fibers, SkeletalMyoblastsProto-Oncogene Proteins c-aktRatsForkhead Box Protein O3FOXO3 protein, humanMicroRNAsMIRN1290 microRNA, humanProto-Oncogene Proteins c-aktAkt/P70/FoxO3AtrophymiR-1290Myoblast differentiation

Identifiers

PMID33722298
PMCPMC7958887
OpenAlexW3135950438

What OpenQuestion holds

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LicenceCC BY
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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.