Evidence map›Paper›PMID 34031457›Full record

ArticleScientific reports2021

Activation of IGF-1 pathway and suppression of atrophy related genes are involved in Epimedium extract (icariin) promoted C2C12 myotube hypertrophy.

Yi-An Lin, Yan-Rong Li, Yi-Ching Chang, Mei-Chich Hsu, Szu-Tah Chen

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
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  6. Mechanism of Qigu capsule as a treatment for sarcopenia based on network pharmacology and experimental validation.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025
    Article
  7. Article
  8. Article
  9. Review
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  11. Article
  12. Angiotensin-(1-7) improves skeletal muscle regeneration.European journal of translational myology · 2023
    Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Nutrients · 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

5 authors at 4 institutions in 1 country.

Yi-An LinDepartment of Sports Medicine, Kaohsiung Medical University, Kaohsiung City, Taiwan.
Yan-Rong LiDivision of Endocrinology and Metabolism, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan City, Taiwan.
Yi-Ching ChangDivision of Endocrinology and Metabolism, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan City, Taiwan.
Mei-Chich HsuDepartment of Sports Medicine, Kaohsiung Medical University, Kaohsiung City, Taiwan. meichich@gmail.com.
Szu-Tah ChenDivision of Endocrinology and Metabolism, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan City, Taiwan. stc1105@cgmh.org.tw.
Chang Gung University · TWChang Gung Memorial Hospital · TWKaohsiung Medical University · TWNational Taiwan Sport University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The regenerative effect of Epimedium and its major bioactive flavonoid icariin (ICA) have been documented in traditional medicine, but their effect on sarcopenia has not been evaluated. The aim of this study was to investigate the effects of Epimedium extract (EE) on skeletal muscle as represented by differentiated C2C12 cells. Here we demonstrated that EE and ICA stimulated C2C12 myotube hypertrophy by activating several, including IGF-1 signal pathways. C2C12 myotube hypertrophy was demonstrated by enlarged myotube and increased myosin heavy chains (MyHCs). In similar to IGF-1, EE/ICA activated key components of the IGF-1 signal pathway, including IGF-1 receptor. Pre-treatment with IGF-1 signal pathway specific inhibitors such as picropodophyllin, LY294002, and rapamycin attenuated EE induced myotube hypertrophy and MyHC isoform overexpression. In a different way, EE induced MHyC-S overexpression can be blocked by AMPK, but not by mTOR inhibitor. On the level of transcription, EE suppressed myostatin and MRF4 expression, but did not suppress atrogenes MAFbx and MuRF1 like IGF-1 did. Differential regulation of MyHC isoform and atrogenes is probably due to inequivalent AKT and AMPK phosphorylation induced by EE and IGF-1. These findings suggest that EE/ICA stimulates pathways partially overlapping with IGF-1 signaling pathway to promote myotube hypertrophy.

Indexed as

AnimalsCell DifferentiationCell LineChromonesFlavonoidsGene Expression RegulationHypertrophyInsulin-Like Growth Factor IMiceMorpholinesMyoblastsMyosin Heavy ChainsPodophyllotoxinSignal TransductionSirolimus2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesFlavonoidsicariininsulin-like growth factor-1, mouseInsulin-Like Growth Factor IMorpholinesMyosin Heavy ChainspicropodophyllinPodophyllotoxinSirolimus

Identifiers

PMID34031457
PMCPMC8144409
OpenAlexW3165760367

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Registered trials

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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.