Evidence map›Paper›PMID 35600773›Full record

ArticleJournal of ginseng research2022

Ginsenoside compound K ameliorates palmitate-induced atrophy in C2C12 myotubes via promyogenic effects and AMPK/autophagy-mediated suppression of endoplasmic reticulum stress.

Tae Jin Kim, Do Hyeon Pyun, Myeong Jun Kim, Ji Hoon Jeong, A M Abd El-Aty, Tae Woo Jung

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Journal of ginseng research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

12 citing papers in PubMed, 35 citations in OpenAlex.

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  9. Therapeutic Applications of Ginseng Natural Compounds for Health Management.International journal of molecular sciences · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 4 countries.

Tae Jin KimDepartment of Pharmacology, College of Medicine, Chung-Ang University, Seoul, Republic of Korea.
Do Hyeon PyunDepartment of Pharmacology, College of Medicine, Chung-Ang University, Seoul, Republic of Korea.
Myeong Jun KimDepartment of Pharmacology, College of Medicine, Chung-Ang University, Seoul, Republic of Korea.
Ji Hoon JeongDepartment of Pharmacology, College of Medicine, Chung-Ang University, Seoul, Republic of Korea.
A M Abd El-AtyState Key Laboratory of Biobased Material and Green Papermaking, College of Food Science and Engineering, Qilu University of Technology, Shandong Academy of Science, Jinan, China.
Tae Woo JungDepartment of Pharmacology, College of Medicine, Chung-Ang University, Seoul, Republic of Korea.
Chung-Ang University · KRCairo University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Compound K (CK) is among the protopanaxadiol (PPD)-type ginsenoside group, which produces multiple pharmacological effects. Herein, we examined the effects of CK on muscle atrophy under hyperlipidemic conditions along with its pro-myogenic effects. Further, the molecular pathways underlying the effects of CK on skeletal muscle have been justified. Methods: C2C12 myotubes were treated with palmitate and CK. C2C12 myoblasts were differentiated using CK for 4-5 days. For the Results: CK treatment attenuated ER stress markers, such as eIF2α phosphorylation and CHOP expression and impaired myotube formation in palmitate-treated C2C12 myotubes and skeletal muscle of mice fed on HFD. CK treatment augmented AMPK along with autophagy markers in skeletal muscle cells Conclusion: These findings denote that CK prevents lipid-induced skeletal muscle apoptosis via AMPK/autophagy-mediated attenuation of ER stress and induction of myoblast differentiation. Therefore, we may suggest the use of CK as a potential therapeutic approach for treating muscle-wasting conditions associated with obesity.

Indexed as

AMPKAutophagyCompound KER stressMyogenesisSarcopenia

Identifiers

PMID35600773
PMCPMC9120645
OpenAlexW3200005232

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.