Evidence map›Paper›PMID 35534947›Full record

ArticleCell proliferation2022

Ginsenoside Rh2 mitigates doxorubicin-induced cardiotoxicity by inhibiting apoptotic and inflammatory damage and weakening pathological remodelling in breast cancer-bearing mice.

Jingang Hou, Yeejin Yun, Changhao Cui, Sunchang Kim

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell proliferation, 2022. 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
5.7field-weighted citation impact, top 3% 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, 37 citations in OpenAlex.

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  11. Unraveling links between aging, circadian rhythm and cancer: Insights from evidence-based analysis.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2024
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  18. Endothelial-to-Mesenchymal Transition: Potential Target of Doxorubicin-Induced Cardiotoxicity.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2023
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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

4 authors at 3 institutions in 1 country.

Jingang HouIntelligent Synthetic Biology Center, Daejeon, Republic of Korea.
Yeejin YunDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, South Korea.
Changhao CuiResearch and Development Team 4, Sempio Foods Company, Cheongju, South Korea.
Sunchang KimIntelligent Synthetic Biology Center, Daejeon, Republic of Korea.ORCID https://orcid.org/0000-0003-0238-7205
Korea Advanced Institute of Science and Technology · KRIntelligent Synthetic Biology Center · KRPohang Iron and Steel (South Korea) · KR

Funding

Advancement of Active Biomedical material Project, funded by the Ministry of Trade P0014633Development of industrialization technology for crop virus and pest Project, funded by the Ministry of Agriculture, Food and Rural Affairs 321109041SB010Intelligent Synthetic Biology Center of the Global Frontier Project, funded by the Ministry of Education, Science and Technology 2011-0031955KAIST Cross-Generation Collaborative Lab projectMulti-Department Research and Business Development Program, funded by Sejong city 2021-153-0028-0019-002BThe Bio-Synergy Research Project of the Ministry of Science, ICT and Future Planning through the National Research Foundation NRF-2021M3A9C4001028
6 · The paper itself

Abstract

objectivesThere are presently a few viable ways to reduce cardiotoxicity of doxorubicin (Dox). The combination of chemotherapy agents with natural compounds delivers greater efficacy and reduces adverse effects in recent researches for cancer treatment. Here, we examined the potential effect of ginsenoside Rh2 on a Dox-based regimen in chemotherapy treatment. MATERIALS AND

methodsHuman breast tumour (MDA-MB-231) xenograft nude mice, human cardiac ventricle fibroblasts, and human umbilical vein endothelial cells (HUVEC) were employed in the present study. Histology, immunohistochemistry, immunofluorescence, western blot, antibody array, and RNA-sequencing analyses were utilized to assess the protective effect of Rh2 on cardiotoxicity induced by Dox and the underlying mechanisms.

resultsRh2-reduced cardiotoxicity by inhibiting the cardiac histopathological changes, apoptosis and necrosis, and consequent inflammation. Pathological remodelling was attenuated by reducing fibroblast to myofibroblast transition (FMT) and endothelial-mesenchymal transition (EndMT) in hearts. RNA-sequencing analysis showed that Dox treatment predominantly targets cell cycle and attachment of microtubules and boosted tumour necrosis, chemokine and interferon-gamma production, response to cytokine and chemokine, and T cell activation, whereas Rh2 regulated these effects. Intriguingly, Rh2 also attenuated fibrosis via promoting senescence in myofibroblasts and reversing established myofibroblast differentiation in EndMT.

conclusionsRh2 regulates multiple pathways in the Dox-provoked heart, proposing a potential candidate for cancer supplement and therapy-associated cardiotoxicity.

Indexed as

Breast NeoplasmsCardiotoxicityAnimalsApoptosisDoxorubicinEndothelial CellsFemaleGinsenosidesHumansMiceMice, NudeMyocytes, CardiacNecrosisOxidative StressRNADoxorubicinginsenoside Rh2GinsenosidesRNA

Identifiers

PMID35534947
PMCPMC9201376
OpenAlexW4229443739

What Socratic 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 Socratic graph.