ReviewCurrent hypertension reports2009
Activation of the ubiquitin-proteasome system in doxorubicin cardiomyopathy.
Review in Current hypertension reports, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 61 citations in OpenAlex.
- Anthracyclines disaggregate and restore mutant p63 function: a potential therapeutic approach for AEC syndrome.Cell death discovery · 2025Article
- Exploring Anthracycline-Induced Cardiotoxicity from the Perspective of Protein Quality Control.Reviews in cardiovascular medicine · 2024Review
- Doxorubicin-induced cardiotoxicity and risk factors.International journal of cardiology. Heart & vasculature · 2024Article
- DoxoDB: A Database for the Expression Analysis of Doxorubicin-Induced lncRNA Genes.Non-coding RNA · 2023Article
- Review
- Anthracycline-induced cardiotoxicity: targeting high-density lipoproteins to limit the damage?Lipids in health and disease · 2022Review
- Tripartite motif 25 ameliorates doxorubicin-induced cardiotoxicity by degrading p85α.Cell death & disease · 2022Article
- Anthracycline Cardiotoxicity Is Associated With Elevated β1-Adrenergic Receptor Density.Journal of the American Heart Association · 2022Article
- Possible Susceptibility Genes for Intervention against Chemotherapy-Induced Cardiotoxicity.Oxidative medicine and cellular longevity · 2020Review
- Phosphorylation Modifications Regulating Cardiac Protein Quality Control Mechanisms.Frontiers in physiology · 2020Review
- Updates in Anthracycline-Mediated Cardiotoxicity.Frontiers in pharmacology · 2018Review
- Visfatin mediates doxorubicin resistance in human non-small-cell lung cancer via Akt-mediated up-regulation of ABCC1.Cell proliferation · 2017Article
- Analysis of defective protein ubiquitylation associated to adriamycin resistant cells.Cell cycle (Georgetown, Tex.) · 2017Article
- Doxorubicin attenuates CHIP-guarded HSF1 nuclear translocation and protein stability to trigger IGF-IIR-dependent cardiomyocyte death.Cell death & disease · 2016Article
- Hypoxia can impair doxorubicin resistance of non-small cell lung cancer cells by inhibiting MRP1 and P-gp expression and boosting the chemosensitizing effects of MRP1 and P-gp blockers.Cellular oncology (Dordrecht, Netherlands) · 2016Article
- HECT-Type Ubiquitin E3 Ligase ITCH Interacts With Thioredoxin-Interacting Protein and Ameliorates Reactive Oxygen Species-Induced Cardiotoxicity.Journal of the American Heart Association · 2016Article
- The regulatory mechanisms of myogenin expression in doxorubicin-treated rat cardiomyocytes.Oncotarget · 2015Article
- Proteotoxicity and cardiac dysfunction.Circulation research · 2015Review
- Dissecting the Mechanisms of Doxorubicin and Oxidative Stress-Induced Cytotoxicity: The Involvement of Actin Cytoskeleton and ROCK1.PloS one · 2015Article
- The tell-tale heart: molecular and cellular responses to childhood anthracycline exposure.American journal of physiology. Heart and circulatory physiology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Doxorubicin (Dox) is a very potent anticancer agent, but its use is limited by its dose-dependent, irreversible cardiotoxicity. Despite intensive research efforts, the mechanism of Dox cardiotoxicity remains poorly understood, so very limited means are available for its prevention or effective management. Recent studies have revealed that a therapeutic dose of Dox can activate proteolysis in cardiomyocytes that is mediated by the ubiquitin-proteasome system (UPS), and that the UPS-mediated degradation of a number of pivotal cardiac transcription factors and/or survival factors is enhanced by Dox treatment. These findings suggest that Dox-induced UPS activation may represent a new mechanism underlying Dox cardiotoxicity. Notably, recent experimental studies suggest that proteasome activation promotes cardiac remodeling during hypertension. This review surveys the current literature on the impact of Dox on the UPS and the potential mechanisms by which UPS activation may compromise the heart during Dox therapy.
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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.