Evidence map›Paper›PMID 28384253›Full record

ArticlePloS one2017

Epicatechin elicits MyoD-dependent myoblast differentiation and myogenic conversion of fibroblasts.

Sang-Jin Lee, Young-Eun Leem, Ga-Yeon Go, Younhee Choi, Yoo Jin Song, Insol Kim, Do Yoon Kim, Yong Kee Kim, Dong-Wan Seo, Jong-Sun Kang and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 23% 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, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  5. Article
  6. Review
  7. Article
  8. (-)-Epicatechin Is a Biased Ligand of Apelin Receptor.International journal of molecular sciences · 2022
    Article
  9. Article
  10. Review
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  18. Ginsenoside Rg1 fromJournal of ginseng research · 2017
    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

11 authors at 3 institutions in 1 country.

Sang-Jin LeeResearch Center for Cell Fate Control, College of Pharmacy, Sookmyung Women's University, Seoul, Republic of Korea.
Young-Eun LeemDepartment of Molecular Cell Biology, Single Cell Network Research Center, Sungkyunkwan University School of Medicine, Suwon, Republic of Korea.
Ga-Yeon GoResearch Center for Cell Fate Control, College of Pharmacy, Sookmyung Women's University, Seoul, Republic of Korea.
Younhee ChoiResearch Center for Cell Fate Control, College of Pharmacy, Sookmyung Women's University, Seoul, Republic of Korea.
Yoo Jin SongResearch Center for Cell Fate Control, College of Pharmacy, Sookmyung Women's University, Seoul, Republic of Korea.
Insol KimResearch Center for Cell Fate Control, College of Pharmacy, Sookmyung Women's University, Seoul, Republic of Korea.
Do Yoon KimResearch Center for Cell Fate Control, College of Pharmacy, Sookmyung Women's University, Seoul, Republic of Korea.
Yong Kee KimResearch Center for Cell Fate Control, College of Pharmacy, Sookmyung Women's University, Seoul, Republic of Korea.
Dong-Wan SeoCollege of Pharmacy, Dankook University, Cheonan, Republic of Korea.
Jong-Sun KangDepartment of Molecular Cell Biology, Single Cell Network Research Center, Sungkyunkwan University School of Medicine, Suwon, Republic of Korea.
Gyu-Un BaeResearch Center for Cell Fate Control, College of Pharmacy, Sookmyung Women's University, Seoul, Republic of Korea.
Sookmyung Women's University · KRSungkyunkwan University · KRDankook University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prevention of age-associated reduction in muscle mass and function is required to manage a healthy life. Supplemental (-)-Epicatechin (EC) appears to act as a potential regulator for muscle growth and strength. However, its cellular and molecular mechanisms as a potential muscle growth agent have not been studied well. In the current study, we investigated a role of EC in differentiation of muscle progenitors to gain the molecular insight into how EC regulates muscle growth. EC enhanced myogenic differentiation in a dose-dependent manner through stimulation of promyogenic signaling pathways, p38MAPK and Akt. EC treatment elevated MyoD activity by enhancing its heterodimerization with E protein. Consistently, EC also positively regulated myogenic conversion and differentiation of fibroblasts. In conclusion, EC has a potential as a therapeutic or nutraceutical remedy to treat degenerative muscle diseases or age-related muscle weakness.

Indexed as

AnimalsCatechinCell DifferentiationCell LineMiceMyoblastsMyoD ProteinCatechinMyoD Protein

Identifiers

PMID28384253
PMCPMC5383328
OpenAlexW2604206333

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.