ReviewCell stress & chaperones2024
The mechanism and therapeutic strategies in doxorubicin-induced cardiotoxicity: Role of programmed cell death.
Review in Cell stress & chaperones, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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
16 citing papers in PubMed.
- Glucagon-like peptide-1 receptor agonists are associated with cardiac, cancer- and mortality-related benefits in diabetic patients treated with anthracyclines.European heart journal open · 2026Article
- Review
- Comparative Analysis of Doxorubicin-Induced Cardiotoxicity in Tumor-Bearing and Non-Tumor-Bearing Mouse Models: A Transcriptomic Methodological Study.International journal of molecular sciences · 2026Article
- Butyrate ameliorates doxorubicin-induced heart failure by inhibiting cardiomyocyte ferroptosis through the gut-heart axis.iScience · 2026Article
- Broad-Spectrum Antibiotics Attenuate the Chemotherapeutic Efficacy of Doxorubicin in MDA-MB-468 Breast Cancer Cells.International journal of breast cancer · 2026Article
- Ferroptosis regulation in doxorubicin-induced cardiotoxicity: multi-mechanism interventions and translational strategies.Frontiers in pharmacology · 2026Review
- β-Catenin and AMPK/AKT/FOXO Signaling Mediate Doxorubicin-Induced Senescence and Lipid Accumulation in C2C12 Myoblasts.Biomolecules & therapeutics · 2026Article
- Article
- pH-responsive doxorubicin-loadedRSC advances · 2025Article
- Transferrin receptor 1-targeted polymersomes therapy for colorectal cancer.Materials today. Bio · 2025Article
- Cardioprotective Effects of Simvastatin in Doxorubicin-Induced Acute Cardiomyocyte Injury.International journal of molecular sciences · 2025Article
- Therapeutic Potential of Ginsenosides in Anthracycline-Induced Cardiotoxicity.Molecules (Basel, Switzerland) · 2025Review
- Non-Coding RNAs in the Regulation of Doxorubicin-Induced Cardiotoxicity.Biomolecules · 2025Review
- Regulatory Effects of Zhenxin Formula in Treating Doxorubicin-Induced Heart Failure: Network Pharmacology and Animal Experimental Verification.Drug design, development and therapy · 2025Article
- Mechanistic Insights into Flavonoid Subclasses as Cardioprotective Agents Against Doxorubicin-Induced Cardiotoxicity: A Comprehensive Review.Drug design, development and therapy · 2025Review
- From cancer therapy to cardiac safety: the role of proteostasis in drug-induced cardiotoxicity.Frontiers in pharmacology · 2024Review
Corrections and comments
- Erratum issued
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin (DOX) is the most commonly used anthracycline anticancer agent, while its clinical utility is limited by harmful side effects like cardiotoxicity. Numerous studies have elucidated that programmed cell death plays a significant role in DOX-induced cardiotoxicity (DIC). This review summarizes several kinds of programmed cell death, including apoptosis, pyroptosis, necroptosis, autophagy, and ferroptosis. Furthermore, oxidative stress, inflammation, and mitochondrial dysfunction are also important factors in the molecular mechanisms of DIC. Besides, a comprehensive understanding of specific signal pathways of DIC can be helpful to its treatment. Therefore, the related signal pathways are elucidated in this review, including sirtuin deacetylase (silent information regulator 2 [Sir2]) 1 (SIRT1)/nuclear factor erythroid 2-related factor 2, SIRT1/Klotho, SIRT1/Recombinant Sestrin 2, adenosine monophosphate-activated protein kinase, AKT, and peroxisome proliferator-activated receptor. Heat shock proteins function as chaperones, which play an important role in various stressful situations, especially in the heart. Thus, some of heat shock proteins involved in DIC are also included. Hence, the last part of this review focuses on the therapeutic research based on the mechanisms above.
Indexed as
Identifiers
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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 Socratic graph.