ArticleFree radical biology & medicine2015
Sulforaphane protects the heart from doxorubicin-induced toxicity.
Article in Free radical biology & medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 125 citations in OpenAlex.
- A HeterogeneousInternational journal of molecular sciences · 2026Article
- Effects of Environmental Temperature During Cultivation of Broccoli Microgreens on Hematological Parameters, Molecular Markers, and Myocardial Antioxidant Status in Swiss Mice.Food science & nutrition · 2026Article
- Sulforaphane Synergies with Phytochemicals and Pharmaceuticals: Implications for Healthspan.Medicines (Basel, Switzerland) · 2026Review
- Understanding the distinct role of PI3K(p110Frontiers in cardiovascular medicine · 2026Review
- Dual-mechanism of phytochemicals in cancer therapy: synergistic anti-angiogenic potency in cancer and proangiogenic impact against chemotherapy-induced cytotoxicity in vital organs.Frontiers in pharmacology · 2026Review
- The Role of the Wnt/β-Catenin Pathway in the Modulation of Doxorubicin-Induced Cytotoxicity in Cardiac H9c2 Cells by Sulforaphane and Quercetin.International journal of molecular sciences · 2025Article
- Protein Kinase C Epsilon Overexpression Protects the Heart Against Doxorubicin-Induced Cardiotoxicity Via Activating SIRT1.Cardiovascular toxicology · 2025Article
- Comparative Neurotoxic Effects of Doxorubicin and Sunitinib: An In Vitro Study on Human Dopaminergic Neuronal Cells.Molecules (Basel, Switzerland) · 2025Article
- Oral Sulforaphane Intervention Protects Against Diabetic Cardiomyopathy in db/db Mice: Focus on Cardiac Lipotoxicity and Substrate Metabolism.Antioxidants (Basel, Switzerland) · 2025Article
- RIP3 orchestrates oxidative stress and pyroptosis in doxorubicin-induced cardiotoxicity through regulation of AKT/Nrf2 signaling cascade.Molecular and cellular biochemistry · 2025Article
- Protective Effects of Sulforaphane Preventing Inflammation and Oxidative Stress to Enhance Metabolic Health: A Narrative Review.Nutrients · 2025Review
- Fasting: A Complex, Double-Edged Blade in the Battle Against Doxorubicin-Induced Cardiotoxicity.Cardiovascular toxicology · 2024Review
- Iron homeostasis and ferroptosis in human diseases: mechanisms and therapeutic prospects.Signal transduction and targeted therapy · 2024Review
- Unveiling the Nutritional Veil of Sulforaphane: With a Major Focus on Glucose Homeostasis Modulation.Nutrients · 2024Review
- Shikonin alleviates doxorubicin-induced cardiotoxicity via Mst1/Nrf2 pathway in mice.Scientific reports · 2024Article
- A review of chemotherapeutic drugs-induced arrhythmia and potential intervention with traditional Chinese medicines.Frontiers in pharmacology · 2024Review
- Sulforaphane's Multifaceted Potential: From Neuroprotection to Anticancer Action.Molecules (Basel, Switzerland) · 2023Review
- Sheng-Mai-Yin inhibits doxorubicin-induced ferroptosis and cardiotoxicity through regulation of Hmox1.Aging · 2023Article
- Carvedilol Phenocopies PGC-1α Overexpression to Alleviate Oxidative Stress, Mitochondrial Dysfunction and Prevent Doxorubicin-Induced Toxicity in Human iPSC-Derived Cardiomyocytes.Antioxidants (Basel, Switzerland) · 2023Article
- Nrf2: a dark horse in doxorubicin-induced cardiotoxicity.Cell death discovery · 2023Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Cardiotoxicity is one of the major side effects encountered during cancer chemotherapy with doxorubicin (DOX) and other anthracyclines. Previous studies have shown that oxidative stress caused by DOX is one of the primary mechanisms for its toxic effects on the heart. Since the redox-sensitive transcription factor, Nrf2, plays a major role in protecting cells from the toxic metabolites generated during oxidative stress, we examined the effects of the phytochemical sulforaphane (SFN), a potent Nrf2-activating agent, on DOX-induced cardiotoxicity. These studies were carried out both in vitro and in vivo using rat H9c2 cardiomyoblast cells and wild type 129/sv mice, and involved SFN pretreatment followed by SFN administration during DOX exposure. SFN treatment protected H9c2 cells from DOX cytotoxicity and also resulted in restored cardiac function and a significant reduction in DOX-induced cardiomyopathy and mortality in mice. Specificity of SFN induction of Nrf2 and protection of H9c2 cells was demonstrated in Nrf2 knockdown experiments. Cardiac accumulation of 4-hydroxynonenal (4-HNE) protein adducts, due to lipid peroxidation following DOX-induced oxidative stress, was significantly attenuated by SFN treatment. The respiratory function of cardiac mitochondria isolated from mice exposed to DOX alone was repressed, while SFN treatment with DOX significantly elevated mitochondrial respiratory complex activities. Co-administration of SFN reversed the DOX-associated reduction in nuclear Nrf2 binding activity and restored cardiac expression of Nrf2-regulated genes at both the RNA and protein levels. Together, our results demonstrate for the first time that the Nrf2 inducer, SFN, has the potential to provide protection against DOX-mediated 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.