ArticleCardiovascular toxicology2021
TRIM25 Rescues Against Doxorubicin-Induced Pyroptosis Through Promoting NLRP1 Ubiquitination.
Article in Cardiovascular toxicology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- GBVAM as a Novel NHE1 Inhibitor Alleviates Doxorubicin-Induced Cardiotoxicity via PI3K/Akt/mTOR Pathway.Drug design, development and therapy · 2026Article
- TRIM25: A Global Player of Cell Death Pathways and Promising Target of Tumor-Sensitizing Therapies.Cells · 2025Review
- TRIM25-mediated XRCC1 ubiquitination accelerates atherosclerosis by inducing macrophage M1 polarization and programmed death.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Recent Advances in the Mechanisms of Cell Death and Dysfunction in Doxorubicin Cardiotoxicity.Reviews in cardiovascular medicine · 2023Review
- SARS-CoV-2 infection of polarized human airway epithelium induces necroptosis that causes airway epithelial barrier dysfunction.Journal of medical virology · 2023Article
- The regulatory role and therapeutic application of pyroptosis in musculoskeletal diseases.Cell death discovery · 2022Review
- The emerging role of pyroptosis in pediatric cancers: from mechanism to therapy.Journal of hematology & oncology · 2022Review
- Tripartite motif 25 ameliorates doxorubicin-induced cardiotoxicity by degrading p85α.Cell death & disease · 2022Article
- Propofol protects cardiomyocytes from doxorubicin-induced toxic injury by activating the nuclear factor erythroid 2-related factor 2/glutathione peroxidase 4 signaling pathways.Bioengineered · 2022Article
- Posttranslational Regulation of Inflammasomes, Its Potential as Biomarkers and in the Identification of Novel Drugs Targets.Frontiers in cell and developmental biology · 2022Review
- NLRP3 Inflammasome Activation Enhanced by TRIM25 is Targeted by the NS1 Protein of 2009 Pandemic Influenza A Virus.Frontiers in microbiology · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin (DOX) is an antineoplastic agent that is widely employed in carcinomas, but it can cause cardiotoxicity in clinic. TRIM25 has E3 ubiquitin ligase activities and can ubiquitinate its target proteins. The role of TRIM25 in DOX-induced cardiotoxicity remains unknown. In this study, our results showed that DOX induced pyroptosis of H9c2 cells by TUNEL staining and Western blot assay. Interestingly, TRIM25 was downregulated in DOX-treated H9c2 cells in a time- and dose-dependent manner. TRIM25 attenuated DOX-induced pyroptosis of H9c2 cells. Furthermore, in vitro ubiquitination assay proved that TRIM25 decreased the stability of NLRP1 via promoting the ubiquitination of NLRP1. The rescue experiments confirmed that TRIM25 inhibited DOX-induced H9c2 cells pyroptosis by regulating NLRP1 stability. Animal experiments demonstrated that overexpression of TRIM25 attenuated DOX-induced cardiomyocyte pyroptosis in rats. In summary, TRIM25 exerts its cardioprotective effects by promoting the ubiquitination of NLRP1 in DOX-induced cardiomyocyte pyroptosis, which provides a novel therapeutic strategy for DOX-induced cardiotoxicity.
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