Evidence map›Paper›PMID 37373547›Full record

ArticleInternational journal of molecular sciences2023

COX5A Alleviates Doxorubicin-Induced Cardiotoxicity by Suppressing Oxidative Stress, Mitochondrial Dysfunction and Cardiomyocyte Apoptosis.

Peipei Zhang, Hao Lu, Yuan Wu, Danbo Lu, Chenguang Li, Xiangdong Yang, Zhangwei Chen, Juying Qian, Junbo Ge

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

24 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Doxorubicin-Induced Cytotoxicity in Adipose-Derived Stem Cells Is Associated With Altered SAPK/JNK Signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Article
  4. COX5A induces M2 macrophage polarization in chronic rhinosinusitis with nasal polyps through ROS generation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. FOXO1-NMNAT3 axis dysregulation promotes doxorubicin cardiotoxicity: NADRedox report : communications in free radical research · 2025
    Article
  11. The Role of Mitochondrial Complexes in Liver Diseases.Journal of clinical and translational hepatology · 2025
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
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  18. Review
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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

9 authors at 1 institution in 1 country.

Peipei ZhangDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, National Clinical Research Center for Interventional Medicine, Shanghai 200032, China.
Hao LuDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, National Clinical Research Center for Interventional Medicine, Shanghai 200032, China.
Yuan WuDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, National Clinical Research Center for Interventional Medicine, Shanghai 200032, China.
Danbo LuDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, National Clinical Research Center for Interventional Medicine, Shanghai 200032, China.ORCID 0000-0003-4753-335X
Chenguang LiDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, National Clinical Research Center for Interventional Medicine, Shanghai 200032, China.
Xiangdong YangDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, National Clinical Research Center for Interventional Medicine, Shanghai 200032, China.
Zhangwei ChenDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, National Clinical Research Center for Interventional Medicine, Shanghai 200032, China.
Juying QianDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, National Clinical Research Center for Interventional Medicine, Shanghai 200032, China.
Junbo GeDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, National Clinical Research Center for Interventional Medicine, Shanghai 200032, China.
Fudan University · CN

Funding

National Natural Science Foundation of China 2019YFC0840601 and 2022YFC2407002National Program on Key Basic Research Project of China 2019YFC0840601 and 2022YFC2407002
6 · The paper itself

Abstract

Doxorubicin (DOX) as a chemotherapeutic agent can cause mitochondrial dysfunction and heart failure. COX5A has been described as an important regulator of mitochondrial energy metabolism. We investigate the roles of COX5A in DOX-induced cardiomyopathy and explore the underlying mechanisms. C57BL/6J mice and H9c2 cardiomyoblasts were treated with DOX, and the COX5A expression was assessed. An adeno-associated virus serum type 9 (AAV9) and lenti-virus system were used to upregulate COX5A expression. Echocardiographic parameters, morphological and histological analyses, transmission electron microscope and immunofluorescence assays were used to assess cardiac and mitochondrial function. In a human study, we found that cardiac COX5A expression was dramatically decreased in patients with end-stage dilated cardiomyopathy (DCM) compared to the control group. COX5A was significantly downregulated following DOX stimulation in the heart of mice and H9c2 cells. Reduced cardiac function, decreased myocardium glucose uptake, mitochondrial morphology disturbance, reduced activity of mitochondrial cytochrome

Indexed as

CardiomyopathiesCardiotoxicityDoxorubicinElectron Transport Complex IVAnimalsApoptosisHumansMiceMice, Inbred C57BLMitochondriaMyocytes, CardiacOxidative StressPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktCOX5A protein, humanDoxorubicinElectron Transport Complex IVPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktapoptosisCOX5Adoxorubicinmitochondrial dysfunctionoxidative stress

Identifiers

PMID37373547
PMCPMC10299295
OpenAlexW4381663300

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.