Evidence map›Paper›PMID 32671648›Full record

ArticleJournal of cardiovascular translational research2021

Salidroside Attenuates Doxorubicin-Induced Cardiac Dysfunction Partially Through Activation of QKI/FoxO1 Pathway.

Fangying Yan, Rongchen Liu, Xinyu Zhuang, Ruoshui Li, Haiming Shi, Xiufang Gao

Abstract read
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In one paragraph

Article in Journal of cardiovascular translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

9 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Insight into the Protective Effect of Salidroside against HOxidative medicine and cellular longevity · 2021
    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

6 authors at 2 institutions in 1 country.

Fangying YanDepartment of Cardiology, Huashan Hospital, Fudan University, NO. 12 Middle Wulumuqi Road, Shanghai, 200000, China.
Rongchen LiuDepartment of Cardiology, Huashan Hospital, Fudan University, NO. 12 Middle Wulumuqi Road, Shanghai, 200000, China.
Xinyu ZhuangDepartment of Cardiology, Huashan Hospital, Fudan University, NO. 12 Middle Wulumuqi Road, Shanghai, 200000, China.
Ruoshui LiDepartment of Cardiology, Huashan Hospital, Fudan University, NO. 12 Middle Wulumuqi Road, Shanghai, 200000, China.
Haiming ShiDepartment of Cardiology, Huashan Hospital, Fudan University, NO. 12 Middle Wulumuqi Road, Shanghai, 200000, China. shihaiming_hs@163.com.
Xiufang GaoDepartment of Cardiology, Huashan Hospital, Fudan University, NO. 12 Middle Wulumuqi Road, Shanghai, 200000, China. gaoxf_fudan@126.com.
Huashan Hospital · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Doxorubicin (DOX) is an effective chemotherapy. However, its usage has been associated with adverse effects. Salidroside (SAL) is an antioxidative drug, which confers protective effects against several diseases. Salidroside can attenuate cardiac dysfunction induced by DOX. Quaking (QKI) is identified as a protective factor that can inhibit cardiotoxicity medicated by DOX through the regulation of cardiac circular RNA expression. The present study investigated the role of QKI on the protective effect of SAL in the DOX-induced cardiotoxicity model. Results indicated that SAL attenuated DOX-induced adverse effects, including cardiac dysfunction, weight loss, and reactive oxygen species (ROS) production, and decreased the expression of BAX, caspase 3, and FoxO1. Also, it increased the Mn-SOD2 and QKI expression in vivo and in vitro. Furthermore, QKI knockdown suppressed anti-cardiotoxicity mediated by SAL. In conclusion, the results of the current study show that salidroside attenuates doxorubicin-induced cardiac dysfunction through activation of QKI/FoxO1 pathway.

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsCardiotoxicityCell LineDisease Models, AnimalDoxorubicinForkhead Box Protein O1GlucosidesHeart DiseasesMaleMiceMice, Inbred C57BLMyocytes, CardiacNerve Tissue ProteinsOxidative StressApoptosis Regulatory ProteinsDoxorubicinForkhead Box Protein O1Foxo1 protein, mouseFoxo1 protein, ratGlucosidesNerve Tissue ProteinsPhenolsQk protein, mouseQk protein, ratReactive Oxygen SpeciesrhodiolosideRNA-Binding ProteinsApoptosisDoxorubicinFoxO1QuakingSalidroside

Identifiers

PMID32671648
OpenAlexW3042840969

What OpenQuestion holds

Textmetadata
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.