ArticleAging2010
Trichostatin A accentuates doxorubicin-induced hypertrophy in cardiac myocytes.
Article in Aging, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 52 citations in OpenAlex.
- Doxorubicin-induced hepatotoxicity: a multifaceted pathogenesis from mitochondrial collapse to immune remodeling and epigenetic memory.Archives of toxicology · 2026Review
- Causes and consequences of DNA double-stranded breaks in cardiovascular disease.Molecular and cellular biochemistry · 2025Review
- Anthracycline-Induced Cardiomyopathy in Cancer Survivors: Management and Long-Term Implications.Advances in experimental medicine and biology · 2025Review
- TongGuanWan Alleviates Doxorubicin- and Isoproterenol-Induced Cardiac Hypertrophy and Fibrosis by Modulating Apoptotic and Fibrotic Pathways.International journal of molecular sciences · 2024Article
- Sibjotang Protects against Cardiac Hypertrophy In Vitro and In Vivo.Life (Basel, Switzerland) · 2023Article
- Review
- Date Palm Pollen Extract Avert Doxorubicin-Induced Cardiomyopathy Fibrosis and Associated Oxidative/Nitrosative Stress, Inflammatory Cascade, and Apoptosis-Targeting Bax/Bcl-2 and Caspase-3 Signaling Pathways.Animals : an open access journal from MDPI · 2021Article
- Review on the Role of Epigenetic Modifications in Doxorubicin-Induced Cardiotoxicity.Frontiers in cardiovascular medicine · 2020Review
- The Cardioprotective Mechanism of Phenylaminoethyl Selenides (PAESe) Against Doxorubicin-Induced Cardiotoxicity Involves Frataxin.Frontiers in pharmacology · 2020Article
- Fasting regulates EGR1 and protects from glucose- and dexamethasone-dependent sensitization to chemotherapy.PLoS biology · 2017Article
- The Transcription Profile Unveils the Cardioprotective Effect of Aspalathin against Lipid Toxicity in an In Vitro H9c2 Model.Molecules (Basel, Switzerland) · 2017Article
- Aspalathin Protects the Heart against Hyperglycemia-Induced Oxidative Damage by Up-Regulating Nrf2 Expression.Molecules (Basel, Switzerland) · 2017Article
- 21st Century Cardio-Oncology: Identifying Cardiac Safety Signals in the Era of Personalized Medicine.JACC. Basic to translational science · 2016Article
- Sulforaphane prevents doxorubicin-induced oxidative stress and cell death in rat H9c2 cells.International journal of molecular medicine · 2015Article
- Pharmacokinetics, antitumor and cardioprotective effects of liposome-encapsulated phenylaminoethyl selenide in human prostate cancer rodent models.Pharmaceutical research · 2015Article
- Chemotherapy-Induced Cardiotoxicity: Overview of the Roles of Oxidative Stress.Oxidative medicine and cellular longevity · 2015Review
- Inactivation of Myosin binding protein C homolog in zebrafish as a model for human cardiac hypertrophy and diastolic dysfunction.Journal of the American Heart Association · 2013Article
- Detrimental effect of class-selective histone deacetylase inhibitors during tissue regeneration following hindlimb ischemia.The Journal of biological chemistry · 2013Article
- Histone deacetylase inhibitors (HDACIs): multitargeted anticancer agents.Biologics : targets & therapy · 2013Article
- Quercetin enhances the antitumor activity of trichostatin A through upregulation of p53 protein expression in vitro and in vivo.PloS one · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone deacetylase inhibitors represent a new class of anticancer therapeutics and the expectation is that they will be most effective when used in combination with conventional cancer therapies, such as the anthracycline, doxorubicin. The dose-limiting side effect of doxorubicin is severe cardiotoxicity and evaluation of the effects of combinations of the anthracycline with histone deacetylase inhibitors in relevant models is important. We used a well-established in vitro model of doxorubicin-induced hypertrophy to examine the effects of the prototypical histone deacetylase inhibitor, Trichostatin A. Our findings indicate that doxorubicin modulates the expression of the hypertrophy-associated genes, ventricular myosin light chain-2, the alpha isoform of myosin heavy chain and atrial natriuretic peptide, an effect which is augmented by Trichostatin A. Furthermore, we show that Trichostatin A amplifies doxorubicin-induced DNA double strand breaks, as assessed by γH2AX formation. More generally, our findings highlight the importance of investigating potential side effects that may be associated with emerging combination therapies for cancer.
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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.