ArticleJournal of Zhejiang University. Science. B2024
Cynaroside regulates the AMPK/SIRT3/Nrf2 pathway to inhibit doxorubicin-induced cardiomyocyte pyroptosis.
Article in Journal of Zhejiang University. Science. B, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Imbalance of the Regulated Cell Death and Autophagic Network: A Core Mechanism Driving Toxicological and Ischemic Myocardial Injury and a Target for Intervention with Traditional Chinese Medicine.Cardiovascular toxicology · 2026Review
- IL-15 aggravates cardiac ischemic injury via impairing macrophage efferocytosis and driving inflammation.Journal of Zhejiang University. Science. B · 2026Article
- Targeting NLRP3 inflammasome to mitigate chemotherapy-induced cardiotoxicity: advances in selective inhibitors and natural modulators.Molecular biology reports · 2026Review
- Hydrogen Mitigated Doxorubicin-Induced Liver Injury via Nrf2/HO-1 Pathway Activation.International journal of molecular sciences · 2026Article
- Combinatorial inhibition of IGF2BP3-regulated receptor tyrosine kinases offers a new therapeutic strategy for triple-negative breast cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- Rhapontin activating nuclear factor erythroid 2-related factor 2 to ameliorate Parkinson's disease-associated gastrointestinal dysfunction.World journal of gastroenterology · 2026Article
- Polyphenol-rich Chinese olive extracts attenuate lipid accumulation in HepG2 cells, accompanied by AMPK phosphorylation and miRNA alterations.Frontiers in nutrition · 2026Article
- FoxO3 Activation Alleviates Doxorubicin-Induced Cardiomyopathy by Enhancing Autophagic Flux and Suppressing mTOR/ROS Signalling.Journal of cellular and molecular medicine · 2025Article
- RBPMS2 can inhibit the NLRP3 / caspase-1 / GSDMD signaling pathway to resist pyroptosis in gastric cancer cells.Scientific reports · 2025Article
- Mechanism of myocardial damage induced by doxorubicinWorld journal of cardiology · 2025Article
- Cardiotoxicity of Chemotherapy: A Multi-OMIC Perspective.Journal of xenobiotics · 2025Review
- Improved myocardial mitochondrial energy metabolism in rats with chronic heart failure by modifying fatty acid oxidation using an extract of sand-fired aconite (Jianchang gang processing).Frontiers in pharmacology · 2025Article
- The Nrf Family and Its Cardioprotective Potential: Mechanisms, Functions, and Therapeutic Perspectives.Drug design, development and therapy · 2025Review
- The effects of cynaroside on lipid metabolism and lipid-related diseases: a mechanistic overview.Frontiers in pharmacology · 2025Review
- Mechanistic Insights into Flavonoid Subclasses as Cardioprotective Agents Against Doxorubicin-Induced Cardiotoxicity: A Comprehensive Review.Drug design, development and therapy · 2025Review
- NLRP3 inflammasome as a therapeutic target in doxorubicin-induced cardiotoxicity: role of phytochemicals.Frontiers in pharmacology · 2025Review
- The therapeutic potential of Honeysuckle in cardiovascular disease: an anti-inflammatory intervention strategy.American journal of translational research · 2024Review
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Authors and funding
9 authors.
Funding
Abstract
Doxorubicin (DOX) is a commonly administered chemotherapy drug for treating hematological malignancies and solid tumors; however, its clinical application is limited by significant cardiotoxicity. Cynaroside (Cyn) is a flavonoid glycoside distributed in honeysuckle, with confirmed potential biological functions in regulating inflammation, pyroptosis, and oxidative stress. Herein, the effects of Cyn were evaluated in a DOX-induced cardiotoxicity (DIC) mouse model, which was established by intraperitoneal injections of DOX (5 mg/kg) once a week for three weeks. The mice in the treatment group received dexrazoxane, MCC950, and Cyn every two days. Blood biochemistry, histopathology, immunohistochemistry, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and western blotting were conducted to investigate the cardioprotective effects and potential mechanisms of Cyn treatment. The results demonstrated the significant benefits of Cyn treatment in mitigating DIC; it could effectively alleviate oxidative stress to a certain extent, maintain the equilibrium of cell apoptosis, and enhance the cardiac function of mice. These effects were realized via regulating the transcription levels of pyroptosis-related genes, such as nucleotide-binding oligomerization domain-like receptor protein 3 (
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