ArticleOxidative medicine and cellular longevity2023
Oxidative Stress and Pyroptosis in Doxorubicin-Induced Heart Failure and Atrial Fibrillation.
Article in Oxidative medicine and cellular longevity, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
- Qishen Yiqi Dripping Pills ameliorate doxorubicin-induced cardiotoxicity: a study based on bioinformatics and experimental verification.Investigational new drugs · 2026Article
- Nuclear Respiratory Factor-1 Ameliorates Heart Failure by Suppressing Cardiomyocyte Pyroptosis-Associated Signaling Via the Downregulation of Gasdermin D and Caspase-1.Cardiology research · 2026Article
- Butyrate ameliorates doxorubicin-induced heart failure by inhibiting cardiomyocyte ferroptosis through the gut-heart axis.iScience · 2026Article
- Chemo-/radiotherapy-induced cardiomyopathy: roles of mitochondria and endoplasmic reticulum.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2026Review
- Doxorubicin-Induced Cardiac Remodeling: Mechanisms and Mitigation Strategies.Cardiovascular drugs and therapy · 2026Review
- Growth differentiation factor 11 attenuates doxorubicin-induced cardiotoxicity by inhibiting myocardial pyroptosis and oxidative stress.Molecular and cellular biochemistry · 2026Article
- Doxorubicin-induced cardiotoxicity: Is ferroptosis the primary driver or a downstream amplifier?EXCLI journal · 2026Review
- An integrated multi-omics study of key mediators and therapeutic targets for doxorubicin-induced atrial fibrillation.PloS one · 2026Article
- Nanomedicine-Based Strategies for Mitigating Chemo/Radiotherapy-Induced Cardiac Inflammation and Fibrosis.Cardiovascular toxicology · 2025Review
- Targeting the NLRP3 by Natural Compounds: Therapeutic Strategies to Mitigate Doxorubicin-Induced Cardiotoxicity.Cell biochemistry and biophysics · 2025Review
- Lycium barbarum Glycopeptide Alleviates Neomycin-Induced Ototoxicity by Inhibiting Tryptophan Hydroxylase-Mediated Serotonin Biosynthesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Angiogenesis in Atrial Fibrillation: A Literature Review.Biomedicines · 2025Review
- NADPH Oxidases in Cancer Therapy-Induced Cardiotoxicity: Mechanisms and Therapeutic Approaches.Cardiovascular toxicology · 2025Review
- PCSK9 Enhances Cardiac Fibrogenesis via the Activation of Toll-like Receptor and NLRP3 Inflammasome Signaling.International journal of molecular sciences · 2025Article
- Active ingredients of traditional Chinese medicine inhibit NOD-like receptor protein 3 inflammasome: a novel strategy for preventing and treating heart failure.Frontiers in immunology · 2025Review
- Bioinformatics analysis of ferroptosis-related biomarkers and potential drug predictions in doxorubicin-induced cardiotoxicity.Frontiers in cardiovascular medicine · 2025Article
- Pyroptosis in cardiovascular diseases: molecular mechanisms, pathological roles, and therapeutic implications.American journal of cardiovascular disease · 2025Review
- Trace elements and metal nanoparticles: mechanistic approaches to mitigating chemotherapy-induced toxicity-a review of literature evidence.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024Review
- The mechanism and therapeutic strategies in doxorubicin-induced cardiotoxicity: Role of programmed cell death.Cell stress & chaperones · 2024Review
- Aerobic Exercise Attenuates Doxorubicin-Induced Cardiomyopathy by Suppressing NLRP3 Inflammasome Activation in a Rat Model.International journal of molecular sciences · 2024Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Patients undergoing doxorubicin (Dox) chemotherapy often develop new-onset atrial fibrillation and heart failure. Recent studies indicate that the TLR4/MyD88/NLRP3 pyroptosis signaling pathway plays a key role in the occurrence and development of cancer, heart failure, and atherosclerosis. However, few studies investigated the role of oxidative stress and pyroptosis in doxorubicin-induced heart failure and new-onset atrial fibrillation. In this study, we recruited 84 healthy subjects, 112 patients undergoing Dox chemotherapy showing heart failure (HF), and 62 patients undergoing Dox treatment who manifested atrial fibrillation (AF). The mRNA and protein levels of TLR4 expression, several downstream pyroptosis-associated proteins (cleaved caspase-1, NLRP3, GSDMD-N, and HMGB-1), serum inflammatory factors, and oxidative stress were detected at the beginning of chemotherapy and after 3 months of Dox chemotherapy. Oxidative stress and downstream pyroptosis-associated proteins tended to increase in the Dox-baseline group to the Dox-HF group. However, virtually no change in the expression of either oxidative stress or pyroptosis-associated proteins was detected in patients after three months of Dox chemotherapy compared with those at baseline. This study suggests that the prolonged oxidative stress and high levels of pyroptosis-associated proteins contribute to cardiac systolic dysfunction, suggesting TLR4 as a novel biomarker and a potential treatment target for doxorubicin-induced heart failure.
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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 Socratic graph.