ArticleOncotarget2017
Astragalus polysaccharide restores autophagic flux and improves cardiomyocyte function in doxorubicin-induced cardiotoxicity.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.
- The Role of mTOR in the Doxorubicin-Induced Cardiotoxicity: A Systematic Review.Cell biochemistry and biophysics · 2025Pooled it
- Autophagic therapeutic targeting for Doxorubicin-induced cardiomyopathy.Molecular biology reports · 2026Review
- Efficacy and Safety of Yiqi Traditional Chinese Medicine Injections for Chronic Pulmonary Heart Disease: A Systematic Review With Pairwise Meta-Analyses and Indirect Comparisons.Pulmonary circulation · 2026Review
- Research Progress on the Role of Traditional Chinese Medicine in Regulating Ferroptosis in Cardiovascular Diseases.Biology · 2026Review
- Qizaobaoxin Decoction ameliorates doxorubicin/trastuzumab-induced cardiotoxicity by modulating gut microbiota and associated metabolites.MedScience · 2026Article
- Mechanisms of astragalus polysaccharide enhancing STM2457 therapeutic efficacy in mMedical oncology (Northwood, London, England) · 2026Article
- Astragalus Polysaccharide Enhances Mitochondrial Biogenesis and Function in Cardiomyocytes Through AMPK Activation.Arquivos brasileiros de cardiologia · 2026Article
- Urolithin A Alleviates Doxorubicin-Induced Senescence in Mesenchymal Stem Cells.International journal of molecular sciences · 2025Article
- Therapeutic potential and mechanisms of traditional Chinese medicine in regulating energy metabolism imbalance in heart failure.Chinese herbal medicines · 2025Review
- FoxO3 Activation Alleviates Doxorubicin-Induced Cardiomyopathy by Enhancing Autophagic Flux and Suppressing mTOR/ROS Signalling.Journal of cellular and molecular medicine · 2025Article
- Doxorubicin-Induced Cardiotoxicity: A Comprehensive Update.Journal of cardiovascular development and disease · 2025Review
- Article
- Natural Products From Traditional Chinese Medicine: Potential Therapeutic Agents in Cancer Therapy-Induced Cardiotoxicity.Drug design, development and therapy · 2025Review
- Astaxanthin mitigates doxorubicin-induced cardiotoxicity via inhibiting ferroptosis and autophagy: a study based on bioinformatic analysis andFrontiers in pharmacology · 2025Article
- Astragalus polysaccharides: structure-immunomodulation relationships, multi-target pharmacological activities, and cutting-edge applications in immune modulation.Frontiers in immunology · 2025Review
- Astragalus polyphenols attenuates doxorubicin-induced cardiotoxicity by activating the PI3K/AKT/NRF2 pathway.PloS one · 2025Article
- The significance of the apelinergic system in doxorubicin-induced cardiotoxicity.Heart failure reviews · 2024Review
- Natural Products for Preventing and Managing Anthracycline-Induced Cardiotoxicity: A Comprehensive Review.Cells · 2024Review
- DEAD-box helicase 17 (DDX17) protects cardiac function by promoting mitochondrial homeostasis in heart failure.Signal transduction and targeted therapy · 2024Article
- The dual functions of the pentacyclic triterpenoid madecassic acid in ameliorating doxorubicin-induced cardiotoxicity and enhancing the antitumor efficacy of doxorubicin.International journal of biological sciences · 2024Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin (adriamycin), an anthracycline antibiotic, is commonly used to treat many types of solid and hematological malignancies. Unfortunately, clinical usage of doxorubicin is limited due to the associated acute and chronic cardiotoxicity. Previous studies demonstrated that Astragalus polysaccharide (APS), the extracts of Astragalus membranaceus, had strong anti-tumor activities and anti-inflammatory effects. However, whether APS could mitigate chemotherapy-induced cardiotoxicity is unclear thus far. We used a doxorubicin-induced neonatal rat cardiomyocyte injury model and a mouse heart failure model to explore the function of APS. GFP-LC3 adenovirus-mediated autophagic vesicle assays, GFP and RFP tandemly tagged LC3 (tfLC3) assays and Western blot analyses were performed to analyze the cell function and cell signaling changes following APS treatment in cardiomyocytes. First, doxorubicin treatment led to C57BL/6J mouse heart failure and increased cardiomyocyte apoptosis, with a disturbed cell autophagic flux. Second, APS restored autophagy in doxorubicin-treated primary neonatal rat ventricular myocytes and in the doxorubicin-induced heart failure mouse model. Third, APS attenuated doxorubicin-induced heart injury by regulating the AMPK/mTOR pathway. The mTOR inhibitor rapamycin significantly abrogated the protective effect of APS. These results suggest that doxorubicin could induce heart failure by disturbing cardiomyocyte autophagic flux, which may cause excessive cell apoptosis. APS could restore normal autophagic flux, ameliorating doxorubicin-induced cardiotoxicity by regulating the AMPK/mTOR pathway.
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