Evidence map›Paper›PMID 31511497›Full record

ArticleCell death & disease2019

miR-146a attenuates apoptosis and modulates autophagy by targeting TAF9b/P53 pathway in doxorubicin-induced cardiotoxicity.

Jian-An Pan, Yong Tang, Jian-Ying Yu, Hui Zhang, Jun-Feng Zhang, Chang-Qian Wang, Jun Gu

Abstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
–field-weighted citation impact
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

69 citing papers in PubMed.

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  16. Evaluation of miR-146a as a potential biomarker for diagnosis of cardiotoxicity induced by chemotherapy in patients with breast cancer.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2025
    Article
  17. Article
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  19. The Potential of Mesenchymal Stem Cell-Derived Exosomes in Cardiac Repair.International journal of molecular sciences · 2024
    Review
  20. Review

9 more citing papers are in PubMed but not listed here.

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

7 authors.

Jian-An PanDepartment of Cardiology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People's Republic of China.
Yong TangDepartment of Hematology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People's Republic of China.
Jian-Ying YuDepartment of Cardiology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People's Republic of China.
Hui ZhangDepartment of Cardiology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People's Republic of China.
Jun-Feng ZhangDepartment of Cardiology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People's Republic of China.
Chang-Qian WangDepartment of Cardiology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People's Republic of China.
Jun GuDepartment of Cardiology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People's Republic of China. gjforsub@163.com.ORCID http://orcid.org/0000-0002-1847-7304

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clinical therapy of doxorubicin (DOX) is limited due to its cardiotoxicity. miR-146a was proved as a protective factor in many cardiovascular diseases, but its role in chronic DOX-induced cardiotoxicity is unclear. The objective of this study was to demonstrate the role of miR-146a in low-dose long-term DOX-induced cardiotoxicity. Experiments have shown that DOX intervention caused a dose-dependent and time-dependent cardiotoxicity involving the increased of apoptosis and dysregulation of autophagy. The cardiotoxicity was inhibited by overexpressed miR-146a and was more severe when miR-146a was downgraded. Further research proved that miR-146a targeted TATA-binding protein (TBP) associated factor 9b (TAF9b), a coactivator and stabilizer of P53, indirectly destroyed the stability of P53, thereby inhibiting apoptosis and improving autophagy in cardiomyocytes. Besides, miR-146a knockout mice were used for in vivo validation. In the DOX-induced model, miR-146a deficiency made it worse whether in cardiac function, cardiomyocyte apoptosis or basal level of autophagy, than wild-type. In conclusion, miR-146a partially reversed the DOX-induced cardiotoxicity by targeting TAF9b/P53 pathway to attenuate apoptosis and adjust autophagy levels.

Indexed as

3' Untranslated RegionsAnimalsApoptosisAutophagyCardiotoxicityCell LineCell SurvivalDoxorubicinHeart InjuriesHumansMaleMiceMice, KnockoutMicroRNAsMicroscopy, Electron, TransmissionMyocytes, Cardiac3' Untranslated RegionsDoxorubicinMicroRNAsMIRN146 microRNA, humanMirn146 microRNA, mouseTAF9b protein, humanTAF9b protein, mouseTATA-Binding Protein Associated FactorsTranscription Factor TFIIDTumor Suppressor Protein p53

Identifiers

PMID31511497
PMCPMC6739392

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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.