Evidence map›Paper›PMID 32918384›Full record

ArticleJournal of cellular and molecular medicine2020

Doxorubicin cardiomyopathy is ameliorated by acacetin via Sirt1-mediated activation of AMPK/Nrf2 signal molecules.

Wei-Yin Wu, Yu-Kai Cui, Yi-Xiang Hong, Yun-Da Li, Yao Wu, Gang Li, Gui-Rong Li, Yan Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
6.1field-weighted citation impact, top 2% 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

38 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Resveratrol Activates SIRT1 to Inhibit Trophoblast Pyroptosis in Preeclampsia.Reproductive sciences (Thousand Oaks, Calif.) · 2025
    Article
  5. Article
  6. Review
  7. Article
  8. Cardioprotective Potential ofCurrent pharmaceutical biotechnology · 2025
    Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  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

8 authors at 1 institution in 1 country.

Wei-Yin WuXiamen Cardiovascular Hospital, Xiamen University, Xiamen, China.
Yu-Kai CuiXiamen Cardiovascular Hospital, Xiamen University, Xiamen, China.
Yi-Xiang HongXiamen Cardiovascular Hospital, Xiamen University, Xiamen, China.
Yun-Da LiXiamen Cardiovascular Hospital, Xiamen University, Xiamen, China.
Yao WuXiamen Cardiovascular Hospital, Xiamen University, Xiamen, China.
Gang LiXiamen Cardiovascular Hospital, Xiamen University, Xiamen, China.
Gui-Rong LiXiamen Cardiovascular Hospital, Xiamen University, Xiamen, China.ORCID 0000-0002-9437-2280
Yan WangXiamen Cardiovascular Hospital, Xiamen University, Xiamen, China.
First Affiliated Hospital of Xiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Doxorubicin cardiotoxicity is frequently reported in patients undergoing chemotherapy. The present study investigates whether cardiomyopathy induced by doxorubicin can be improved by the natural flavone acacetin in a mouse model and uncovers the potential molecular mechanism using cultured rat cardiomyoblasts. It was found that the cardiac dysfunction and myocardial fibrosis induced by doxorubicin were significantly improved by acacetin in mice with impaired Nrf2/HO-1 and Sirt1/pAMPK molecules, which is reversed by acacetin treatment. Doxorubicin decreased cell viability and increased ROS production in rat cardiomyoblasts; these effects are significantly countered by acacetin (0.3-3 μM) in a concentration-dependent manner via activating Sirt1/pAMPK signals and enhancing antioxidation (Nrf2/HO-1 and SOD1/SOD2) and anti-apoptosis. These protective effects were abolished in cells with silencing Sirt1. The results demonstrate for the first time that doxorubicin cardiotoxicity is antagonized by acacetin via Sirt1-mediated activation of AMPK/Nrf2 signal molecules, indicating that acacetin may be a drug candidate used clinically for protecting against doxorubicin cardiomyopathy.

Indexed as

Signal TransductionAMP-Activated Protein KinasesAnimalsAntioxidantsApoptosisCardiomyopathiesCardiotonic AgentsCell LineCell SurvivalDoxorubicinFlavonesGene SilencingHeart VentriclesMaleMice, Inbred C57BLMyocardiumacacetinAMP-Activated Protein KinasesAntioxidantsCardiotonic AgentsDoxorubicinFlavonesNF-E2-Related Factor 2Reactive Oxygen SpeciesSirtuin 1acacetinantioxidantcardiotoxicitydoxorubicinoxidative stressSirt1

Identifiers

PMID32918384
PMCPMC7579684
OpenAlexW3086543504

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.