Evidence map›Paper›PMID 29434790›Full record

ArticleExperimental and therapeutic medicine2018

Cyanidin ameliorates cisplatin-induced cardiotoxicity via inhibition of ROS-mediated apoptosis.

Peng Qian, Li-Jie Yan, Yong-Qiang Li, Hai-Tao Yang, Hong-Yan Duan, Jin-Tao Wu, Xian-Wei Fan, Shan-Ling Wang

Open access · diamondAbstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 59 citations in OpenAlex.

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  4. Chemo-/radiotherapy-induced cardiomyopathy: roles of mitochondria and endoplasmic reticulum.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2026
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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

8 authors at 1 institution in 1 country.

Peng QianDepartment of Cardiology, Henan Provincial People's Hospital, Zhengzhou, Henan 450003, P.R. China.
Li-Jie YanDepartment of Cardiology, Henan Provincial People's Hospital, Zhengzhou, Henan 450003, P.R. China.
Yong-Qiang LiDepartment of Cardiology, Henan Provincial People's Hospital, Zhengzhou, Henan 450003, P.R. China.
Hai-Tao YangDepartment of Cardiology, Henan Provincial People's Hospital, Zhengzhou, Henan 450003, P.R. China.
Hong-Yan DuanDepartment of Cardiology, Henan Provincial People's Hospital, Zhengzhou, Henan 450003, P.R. China.
Jin-Tao WuDepartment of Cardiology, Henan Provincial People's Hospital, Zhengzhou, Henan 450003, P.R. China.
Xian-Wei FanDepartment of Cardiology, Henan Provincial People's Hospital, Zhengzhou, Henan 450003, P.R. China.
Shan-Ling WangDepartment of Cardiology, Henan Provincial People's Hospital, Zhengzhou, Henan 450003, P.R. China.
Henan Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress and apoptosis serve an essential role in cisplatin-induced cardiotoxicity, which limits its clinical use, and increases the risk of cardiovascular disease. As a natural drug, the antioxidant and antitumor effects of cyanidin have been recognized, but its protective effect on cisplatin-induced cardiomyocyte cytotoxicity remains unclear. H9c2 cells were treated with cisplatin (1-40 µM) in the presence or absence of cyanidin (40-80 µM), subsequently; oxidative stress, apoptosis and mitochondrial function were assessed using several techniques. The results demonstrated that cyanidin was able to dose-dependently reverse cisplatin-induced cell damage and apoptosis, attenuate the accumulation of reactive oxygen species (ROS), and mitochondrial membrane potential depolarization, downregulate the expression of Bcl-2 homologous antagonist/killer, upregulate the expression of apoptosis regulator Bcl-2, and reduce the activation of caspase 3, caspase 9, but not caspase 8. Furthermore, the results revealed that the translocation of apoptosis regulator Bax (Bax) from the cytoplasm to the mitochondrial membrane serves an essential role in cisplatin-induced apoptosis. Cyanidin was able to block the translocation of Bax and reduce the release of cytochrome

Indexed as

apoptosiscardiotoxicitycisplatincyanidinERK pathwayoxidative stress

Identifiers

PMID29434790
PMCPMC5776514
OpenAlexW2771839740

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.