ArticleCardiovascular research2011
Activation of the aryl hydrocarbon receptor by doxorubicin mediates cytoprotective effects in the heart.
Article in Cardiovascular research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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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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
33 citing papers in PubMed, 60 citations in OpenAlex.
- Aryl Hydrocarbon Receptor (AhR) and Vascular Endothelial Growth Factor (VEGF) Crosstalk in Doxorubicin Nephrotoxicity: Mechanisms and Therapeutic Perspectives.Current issues in molecular biology · 2026Article
- Exploring the mechanism of Yi Qi Huo Xue compound prescription in treating chronic heart failure based on integrated network pharmacology and transcriptomics.Frontiers in cardiovascular medicine · 2026Article
- Uncovering Thyroid Vulnerability to Doxorubicin: Integrative Cellular and in vivo Evidence of Mitochondrial Dysfunction.Drug design, development and therapy · 2026Article
- Protective Effects of Ginsenosides on Drug-induced Cardiotoxicity: A New Therapeutic Approach with Focus on Molecular Mechanisms in Cardio-oncology Field.Current medicinal chemistry · 2026Review
- Aryl Hydrocarbon Receptor in Health and Disease.MedComm · 2025Review
- Parthenolide alleviates doxorubicin-induced cardiotoxicity via regulation ofJournal of traditional and complementary medicine · 2025Article
- Pleiotropic role of CCR9/CCL25 signaling in adriamycin-induced cardiomyopathy.Journal of advanced research · 2025Article
- Protein-Level Analysis of Differential Response to Chemotherapy in Triple-Negative Breast Cancer Identifies CYP1B1 as a Biomarker for Chemotherapy Resistance.Cancer research communications · 2025Article
- Microbiota-indole-3-propionic acid-heart axis mediates the protection of leflunomide against αPD1-induced cardiotoxicity in mice.Nature communications · 2025Article
- Metabolic Side Effects from Antipsychotic Treatment with Clozapine Linked to Aryl Hydrocarbon Receptor (AhR) Activation.Biomedicines · 2024Review
- Kynurenic Acid/AhR Signaling at the Junction of Inflammation and Cardiovascular Diseases.International journal of molecular sciences · 2024Review
- Pretreatment with Indole-3-Propionic Acid Attenuates Lipopolysaccharide-Induced Cardiac Dysfunction and Inflammation Through the AhR/NF-κB/NLRP3 Pathway.Journal of inflammation research · 2024Article
- Investigation of doxorubicin combined with ciprofloxacin-induced cardiotoxicity: from molecular mechanism to fundamental heart function.Naunyn-Schmiedeberg's archives of pharmacology · 2023Article
- Comparison of moderate-intensity continuous training and high-intensity interval training effects on the Ido1-KYN-Ahr axis in the heart tissue of rats with occlusion of the left anterior descending artery.Scientific reports · 2023Article
- Skin Immuno-CometChip in 3D vs. 2D Cultures to Screen Topical Toxins and Skin-Specific Cytochrome Inducers.Genes · 2023Article
- Natural compounds targeting mitochondrial dysfunction: emerging therapeutics for target organ damage in hypertension.Frontiers in pharmacology · 2023Review
- Ongoing Clinical Trials in Aging-Related Tissue Fibrosis and New Findings Related to AhR Pathways.Aging and disease · 2022Review
- Activation of the aryl hydrocarbon receptor by clozapine induces preadipocyte differentiation and contributes to endothelial dysfunction.Journal of psychopharmacology (Oxford, England) · 2022Article
- Gut microbiota-derived indole 3-propionic acid partially activates aryl hydrocarbon receptor to promote macrophage phagocytosis and attenuate septic injury.Frontiers in cellular and infection microbiology · 2022Article
- piR-39980 mediates doxorubicin resistance in fibrosarcoma by regulating drug accumulation and DNA repair.Communications biology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
aimsDoxorubicin (DOX) is a highly effective chemotherapeutic agent; however, cumulative dose-dependent cardiotoxicity is a significant side effect of this therapy. Because DOX is a polyaromatic hydrocarbon, we hypothesized that it will be metabolized by the activation of the aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor that is involved in the metabolism of numerous xenobiotic agents. These studies were performed to determine whether DOX activates AhR and whether this activation modulates the toxicity of DOX in cardiomyocytes. METHODS AND
resultsTreatment with DOX induced AhR migration to the nucleus, increased AhR binding with its co-factor, aryl hydrocarbon receptor nuclear translocator-1 (ARNT1), and increased the expression of AhR-regulated phase I (CYP1A1) and phase II (GSTA1) drug-metabolizing enzymes in both cardiomyocytes and in the intact heart. Knockdown of AhR in H9C2 cells abolished DOX-induced increases in CYP1A1 and GSTA1 expression. Similar results were obtained by treating adult rat ventricular myocytes with the AhR antagonist, CH-223191. Taken together, these findings indicate that DOX-induced upregulation of CYP1A1 and GSTA1 expression is AhR dependent. AhR null mice treated with 10 mg/kg DOX did not show any activation of CYP1A1 or GSTA1 expression. Moreover, lack of AhR in vivo resulted in a significant decrease in left ventricular function compared with wild-type animals, and increased p53 activation and apoptosis in the heart after treatment with DOX.
conclusionsThese findings indicate that AhR plays an important role in DOX metabolism by the heart and further demonstrate that AhR is cardioprotective against DOX-induced cardiotoxicity.
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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.