Evidence map›Paper›PMID 31225944›Full record

ArticleJournal of cellular and molecular medicine2019

Yellow Wine Polyphenolic Compounds prevents Doxorubicin-induced cardiotoxicity through activation of the Nrf2 signalling pathway.

Hui Lin, Jie Zhang, Tingjuan Ni, Na Lin, Liping Meng, Feidan Gao, Hangqi Luo, Xiatian Liu, Jufang Chi, Hangyuan Guo

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  17. Frontiers in pharmacology · 2023
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  18. Article
  19. Review
  20. 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

10 authors at 4 institutions in 1 country.

Hui LinDepartment of Cardiology, Shaoxing People's Hospital (Shaoxing Hospital, Zhejiang University School of Medicine), Shaoxing, China.
Jie ZhangThe First Clinical Medical College, Wenzhou Medical University, Wenzhou, China.
Tingjuan NiZhejiang University School of Medicine, Hangzhou, China.
Na LinZhejiang Chinese Medical University, Hangzhou, China.
Liping MengDepartment of Cardiology, Shaoxing People's Hospital (Shaoxing Hospital, Zhejiang University School of Medicine), Shaoxing, China.
Feidan GaoZhejiang Chinese Medical University, Hangzhou, China.
Hangqi LuoZhejiang University School of Medicine, Hangzhou, China.
Xiatian LiuDepartment of Ultrasound, Shaoxing People's Hospital (Shaoxing Hospital, Zhejiang University School of Medicine), Shaoxing, China.
Jufang ChiDepartment of Cardiology, Shaoxing People's Hospital (Shaoxing Hospital, Zhejiang University School of Medicine), Shaoxing, China.ORCID 0000-0001-9247-1624
Hangyuan GuoDepartment of Cardiology, Shaoxing People's Hospital (Shaoxing Hospital, Zhejiang University School of Medicine), Shaoxing, China.ORCID 0000-0001-5637-6099
Shaoxing People's Hospital · CNWenzhou Medical University · CNZhejiang Chinese Medical University · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Doxorubicin (DOX) is considered as the major culprit in chemotherapy-induced cardiotoxicity. Yellow wine polyphenolic compounds (YWPC), which are full of polyphenols, have beneficial effects on cardiovascular disease. However, their role in DOX-induced cardiotoxicity is poorly understood. Due to their antioxidant property, we have been suggested that YWPC could prevent DOX-induced cardiotoxicity. In this study, we found that YWPC treatment (30 mg/kg/day) significantly improved DOX-induced cardiac hypertrophy and cardiac dysfunction. YWPC alleviated DOX-induced increase in oxidative stress levels, reduction in endogenous antioxidant enzyme activities and inflammatory response. Besides, administration of YWPC could prevent DOX-induced mitochondria-mediated cardiac apoptosis. Mechanistically, we found that YWPC attenuated DOX-induced reactive oxygen species (ROS) and down-regulation of transforming growth factor beta 1 (TGF-β1)/smad3 pathway by promoting nuclear factor (erythroid-derived 2)-like 2 (Nrf2) nucleus translocation in cultured H9C2 cardiomyocytes. Additionally, YWPC against DOX-induced TGF-β1 up-regulation were abolished by Nrf2 knockdown. Further studies revealed that YWPC could inhibit DOX-induced cardiac fibrosis through inhibiting TGF-β/smad3-mediated ECM synthesis. Collectively, our results revealed that YWPC might be effective in mitigating DOX-induced cardiotoxicity by Nrf2-dependent down-regulation of the TGF-β/smad3 pathway.

Indexed as

AnimalsAntibiotics, AntineoplasticAntioxidantsApoptosisCardiomegalyCardiotoxicityCell LineDoxorubicinFibrosisMaleMembrane Potential, MitochondrialMyocytes, CardiacNF-E2-Related Factor 2OryzaOxidative StressPolyphenolsAntibiotics, AntineoplasticAntioxidantsDoxorubicinNfe2l2 protein, ratNF-E2-Related Factor 2PolyphenolsReactive Oxygen SpeciesSmad3 ProteinSmad3 protein, ratTransforming Growth Factor beta1cardiotoxicitydoxorubicinNrf2oxidative stresspolyphenols

Identifiers

PMID31225944
PMCPMC6714138
OpenAlexW2952571707

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.