Evidence map›Paper›PMID 37232350›Full record

ArticleInternational journal of molecular medicine2023

Ginsenoside Rg1 regulates autophagy and endoplasmic reticulum stress via the AMPK/mTOR and PERK/ATF4/CHOP pathways to alleviate alcohol‑induced myocardial injury.

Ge Tian, Jing Li, Lina Zhou

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2023. 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
9.7field-weighted citation impact, top 1% 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, 45 citations in OpenAlex.

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  13. Components ofFrontiers in pharmacology · 2026
    Article
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  16. AMD1, a cardiotoxicity target for Maduramicin.BMC pharmacology & toxicology · 2025
    Article
  17. Article
  18. Cucurbitacin IIa Ameliorates DSS-Induced Ulcerative Colitis via Enhancing Intestinal Barrier Function and Inhibiting PERK/ATF4/CHOP Signaling Pathway.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2024
    Article
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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

3 authors at 2 institutions in 1 country.

Ge TianDepartment of Cardiology, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning 121000, P.R. China.
Jing LiDepartment of Cardiology, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.
Lina ZhouDepartment of Geriatrics, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning 121000, P.R. China.
Jinzhou Medical University · CNChina Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been reported that ginsenoside Rg1 (G‑Rg1) can alleviate alcoholic liver injury, cardiac hypertrophy and myocardial ischemia, as well as reperfusion injury. Therefore, the present study aimed to investigate the role of G‑Rg1 in alcohol‑induced myocardial injury, as well as to elucidate its underlying mechanisms of action. For this purpose, H9c2 cells were stimulated with ethanol. Subsequently, H9c2 cell viability and apoptosis were determined using a Cell Counting Kit‑8 assay and flow cytometric analysis, respectively. The levels of lactate dehydrogenase and caspase‑3 in the H9c2 cell culture supernatant were detected using corresponding assay kits. In addition, the expression of green fluorescent protein (GFP)‑light chain 3 (LC3) and that of C/EBP homologous protein (CHOP) were evaluated using GFP‑LC3 assay and immunofluorescence staining, respectively. The expression levels of apoptosis‑, autophagy‑, endoplasmic reticulum stress (ERS)‑ and adenosine 5'‑monophosphate‑activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway‑related proteins were detected using western blot analysis. The results revealed that treatment with G‑Rg1 enhanced the viability and suppressed the apoptosis of ethanol‑stimulated H9c2 cells. G‑Rg1 also attenuated autophagy and ERS in ethanol‑stimulated H9c2 cells. In addition, the levels of phosphorylated (p)‑protein kinase R (PKR)‑like ER kinase (PERK), p‑eukaryotic translation initiation factor 2a, activating transcription factor 4 (ATF4), CHOP, caspase‑12 and p‑AMPK were downregulated, while the p‑mTOR level was upregulated in ethanol‑stimulated H9c2 cells treated with G‑Rg1. Furthermore, the co‑treatment of G‑Rg1‑treated ethanol‑stimulated H9c2 cells with AICAR, an AMPK agonist, or CCT020312, a PERK agonist, inhibited cell viability and promoted cell apoptosis, autophagy and ERS. Overall, the results of the present study suggest that G‑Rg1 suppresses autophagy and ERS via inhibiting the AMPK/mTOR and PERK/ATF4/CHOP pathways to alleviate ethanol‑induced H9c2 cell injury.

Indexed as

Activating Transcription Factor 4Heart InjuriesAMP-Activated Protein KinasesAnimalsApoptosisAutophagyEndoplasmic Reticulum StressEthanolGinsenosidesRatsSignal TransductionTOR Serine-Threonine KinasesActivating Transcription Factor 4AMP-Activated Protein KinasesEthanolginsenoside Rg1GinsenosidesTOR Serine-Threonine Kinasesadenosine 5'‑monophosphate‑activated protein kinase/mammalian target of rapamycinautophagyendoplasmic reticulum stressginsenoside Rg1myocardial injuryprotein kinase R (PKR)‑like ER kinase

Identifiers

PMID37232350
PMCPMC10241156
OpenAlexW4377824380

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.