ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2023
The Imbalance of p53-Park7 Signaling Axis Induces Iron Homeostasis Dysfunction in Doxorubicin-Challenged Cardiomyocytes.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 64 citations in OpenAlex.
- BMSC-derived EVs alleviate doxorubicin-induced cardiotoxicity via miR-210-3p involving the ACVR1B-SMAD3-PGC-1α signaling axis.Stem cell research & therapy · 2026Article
- Cardiovascular Toxicity in Cancer Therapy: Potential Mechanisms of Ferroptosis and Treatment Strategies.Cells · 2026Review
- Morroniside Attenuates Doxorubicin-Induced Cardiotoxicity by Activating the PI3K/AKT/Nrf2/HO-1 Pathway to Inhibit Ferroptosis and Oxidative Stress.Journal of biochemical and molecular toxicology · 2026Article
- Risk Factors for Cardiovascular Disease: Epidemiology, Screening, Prevention, and Therapeutic Interventions.MedComm · 2026Review
- Charge-regulated hepatic γ-glutamyltranspeptidase fluorescent probe:Chemical science · 2026Article
- Arachidonate lipoxygenase 5 metabolism axis promoting ferroptosis: a potential druggable target for doxorubicin-induced cardiomyopathy.British journal of cancer · 2026Article
- Ferroptosis in Doxorubicin-Induced Cardiotoxicity: From Molecular Mechanisms to Therapeutic Strategies and Clinical Management Paradigms.Reviews in cardiovascular medicine · 2026Review
- Cysteine imaging reveals early redox dysregulation and identifies gnetol as a ferroptosis-modulating agent in doxorubicin cardiotoxicity.Redox biology · 2026Article
- CD74 deficiency protects against doxorubicin cardiotoxicity through RRM2-mediated regulation of ferroptosis.Acta pharmaceutica Sinica. B · 2026Article
- Targeting ATP11B-YAP axis repairs mitochondrial function and inhibits neuronal ferroptosis to attenuate age-related cognitive decline.Signal transduction and targeted therapy · 2026Article
- Inhibition of SLC11A1-Mediated Lysosomal Iron Accumulation in Microglia Promotes Repair Following White Matter Stroke.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Conducting polymer-stabilized nanozymes alleviate sepsis-induced myocardial injury by inhibiting iron accumulation and lipid peroxidation.Nature communications · 2026Article
- Lithospermic Acid Improves Doxorubicin-Induced Cardiomyopathy Through Sirtuin-3-Mediated Deacetylation of p53.Phytotherapy research : PTR · 2026Article
- FTH1 mRNA-Protein Discordance in Cardiac Ferroptosis: Multilayer Posttranscriptional and Degradative Control.Cardiovascular therapeutics · 2026Review
- Cardiomyocyte programmed cell death in dilated cardiomyopathy: molecular crosstalk and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
- TAK-981 potentiates doxorubicin immunocide in triple-negative breast cancer by IFN I-dependent NK cell stimulation.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- Metabolic Interplay in Acute Lung Injury: PARK7 Integrates FADS1/2-Dependent PUFA Metabolism and H3K14 Lactylation to Attenuate Endothelial Ferroptosis and Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Identification and validation of feature genes of acute myocardial infarction based on ferroptosis-related genes.European journal of medical research · 2025Article
- EBBP-Mediated Integrated Stress Response Attenuates Anthracycline-Induced Cardiotoxicity by Inhibiting the Ferroptosis of Cardiomyocytes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Doxorubicin (DOX)-induced cardiotoxicity (DoIC) is a major side effect for cancer patients. Recently, ferroptosis, triggered by iron overload, is demonstrated to play a role in DoIC. How iron homeostasis is dysregulated in DoIC remains to be elucidated. Here, the authors demonstrate that DOX challenge exhibits reduced contractile function and induction of ferroptosis-related phenotype in cardiomyocytes, evidenced by iron overload, lipid peroxide accumulation, and mitochondrial dysfunction. Compared to Ferric ammonium citrate (FAC) induced secondary iron overload, DOX-challenged cardiomyocytes show a dysfunction of iron homeostasis, with decreased cytoplasmic and mitochondrial iron-sulfur (FeS) cluster-mediated aconitase activity and abnormal expression of iron homeostasis-related proteins. Mechanistically, mass spectrometry analysis identified DOX-treatment induces p53-dependent degradation of Parkinsonism associated deglycase (Park7) which results in iron homeostasis dysregulation. Park7 counteracts iron overload by regulating iron regulatory protein family transcription while blocking mitochondrial iron uptake. Knockout of p53 or overexpression of Park7 in cardiomyocytes remarkably restores the activity of FeS cluster and iron homeostasis, inhibits ferroptosis, and rescues cardiac function in DOX treated animals. These results demonstrate that the iron homeostasis plays a key role in DoIC ferroptosis. Targeting of the newly identified p53-Park7 signaling axis may provide a new approach to prevent DoIC.
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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.