ArticleEvidence-based complementary and alternative medicine : eCAM2022
MiR-199 Aggravates Doxorubicin-Induced Cardiotoxicity by Targeting TAF9b.
Article in Evidence-based complementary and alternative medicine : eCAM, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 5 papers.
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.
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.
Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Mechanisms of ferroptotic and non-ferroptotic organ toxicity of chemotherapy: protective and therapeutic effects of ginger, 6-gingerol and zingerone in preclinical studies.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Exosomes Derived from hucMSCs Primed with IFN-γ Suppress the NF-κB Signal Pathway in LPS-Induced ALI by Modulating the miR-199b-5p/AFTPH Axis.Cell biochemistry and biophysics · 2024Article
- Review
- The beneficial role of exercise in preventing doxorubicin-induced cardiotoxicity.Frontiers in physiology · 2023Review
- Retracted: MiR-199 Aggravates Doxorubicin-Induced Cardiotoxicity by Targeting TAF9b.Evidence-based complementary and alternative medicine : eCAM · 2023Article
Corrections and comments
- Retraction · 2023-12-13Compromised Peer Review · Investigation by Journal/Publisher · Investigation by Third Party · Paper Mill · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The clinical application of doxorubicin (DOX) is limited because of its cardiotoxicity. However, the pathogenic mechanism of DOX and the role of miRNA in DOX-induced cardiotoxicity remain to be further studied. This study aimed to investigate the role of miR-199 in DOX-mediated cardiotoxicity. A mouse model of myocardial cell injury induced by DOX was established. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression changes of miR-199 and TATA-binding protein associated factor 9B (TAF9b) in DOX-induced cardiac injury. Cell apoptosis was detected by TUNEL staining and flow cytometry. The expression levels of apoptosis-related proteins, namely, Bax and Bcl-2, were detected by qPCR. The expression of Beclin-1 and LC3b was detected by western blotting. The binding effect of miR-199 with TAF9b was verified by dual-luciferase reporter gene assay. In this study, overexpression of miR-199 could promote cardiotoxicity. Inhibition of miR-199 could alleviate DOX-mediated myocardial injury. Further studies showed that miR-199 targeted TAF9b. Moreover, miR-199 promoted apoptosis of myocardial cells and aggravated autophagy. Furthermore, we demonstrated that TAF9B knockdown reversed the myocardial protective effect of miR-199 inhibitors. Therefore, miR-199 promoted DOX-mediated cardiotoxicity by targeting TAF9b, thereby aggravating apoptosis and regulating autophagy.
Identifiers
What OpenQuestion holds
Registered trials
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.