ArticleJournal of the American Heart Association2025
Ring Finger Protein 2 Promotes Oxidative Stress and Mitochondrial Dysfunction in Doxorubicin-Induced Cardiotoxicity Via the Mercaptopyruvate Sulfurtransferase/Hydrogen Sulfide Pathway.
Article in Journal of the American Heart Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed.
- Imbalance of the Regulated Cell Death and Autophagic Network: A Core Mechanism Driving Toxicological and Ischemic Myocardial Injury and a Target for Intervention with Traditional Chinese Medicine.Cardiovascular toxicology · 2026Review
- Heart failure induced by cancer therapies: focus on targeted agents, mechanisms, risk prediction, and clinical management.Frontiers in pharmacology · 2026Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDoxorubicin, a broad-spectrum chemotherapy drug, is often associated with dosage-dependent cardiotoxicity, which results in its limited clinical application. A therapeutic dose of doxorubicin can activate cardiac ubiquitin-proteasome system, whereas the role and potential mechanisms of this process in doxorubicin-induced cardiomyopathy (DIC) remain unclear. Herein, we assessed the potential role and therapeutic value of RNF2 (ring finger protein 2) on doxorubicin-induced cardiac damage.
methodsCardiomyocyte-specific RNF2 knockout or overexpression mice received doxorubicin intraperitoneal injection to establish the DIC model. The effects of RNF2 and its downstream mediators were explored through RNA sequencing, immunoprecipitation mass spectrometry analysis, and protein pulldown analysis.
resultsThe expression of RNF2 was significantly increased in doxorubicin-treated murine myocardium and neonatal rat ventricular myocytes. Cardiomyocyte-specific RNF2 overexpression resulted in exaggerated DIC accompanied by increased cardiac dysfunction, fibrosis and apoptosis. Cardiac damage was mitigated in α-myosin heavy chain promoter-driven heterozygous-Cre
conclusionsOur findings reveal the role of RNF2 in oxidative stress and mitochondrial homeostasis and the progression of DIC, suggesting that targeting RNF2 may be a potential therapeutic benefit for DIC.
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