ArticleScientific reports2019
Doxorubicin-induced cardiomyopathy associated with inhibition of autophagic degradation process and defects in mitochondrial respiration.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.
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Who cites it
114 citing papers in PubMed, 180 citations in OpenAlex.
- Priming of human iPSCs with doxorubicin causes genome-wide transcriptional reprogramming and functional impairments in iPSC-derived cardiomyocytes.NPJ Regenerative medicine · 2026Article
- Organelle network dysfunction in primary cardiomyopathy: An integrated perspective on pathogenesis and therapeutics.Journal of molecular and cellular cardiology plus · 2026Review
- From Computational Prediction toResearch square · 2026Article
- Effects of mitochondrial ABCB7 transporter upregulation on acute doxorubicin cardiorespiratory muscle injury.Journal of applied physiology (Bethesda, Md. : 1985) · 2026Article
- Mitochondrial-Targeted SS-31 Attenuates the Doxorubicin-Induced Cardiomyoblast H9C2 Cell Senescence.Biology · 2026Article
- Novel Mechanism of and Therapeutic Approach for Anthracycline-Induced Cardiotoxicity.Cancer research communications · 2026Article
- Neuregulin-1β Mitigates Doxorubicin-Induced Cardiotoxicity viaInternational journal of molecular sciences · 2026Article
- Developing virtual physiology of human tumor tissue for malignancy assessment.NPJ precision oncology · 2026Article
- Determining Preclinical Safety of Aclarubicin in Pediatric Malignancies.Pediatric blood & cancer · 2026Article
- Disruption of ATP Synthase Spatiotemporal Organization, CaAging cell · 2026Article
- A Systemic Selective Modified mRNA Delivery Platform for Preventing Chemotherapy-Induced Cardiotoxicity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- PHB1 Attenuates Triptolide-induced Cardiotoxicity by Regulating Mitochondrial Dynamics in Cultured Newborn Mice Cardiomyocytes.Journal of cardiovascular pharmacology · 2026Article
- Nanoparticle-Based Targeted Drug Delivery Methods for Heart-Specific Distribution in Cardiovascular Therapy.Pharmaceutics · 2025Review
- Ginsenoside Rb1 ameliorates post-doxorubicin treatment myocardial hypertrophy via CaN/NFATc4/GATA4.Journal of ginseng research · 2025Article
- Porphyrinic MOF-derived novel nanocomposite for gastric anticancer and Helicobacter pylori photoantibacterial effect assay.Scientific reports · 2025Article
- Mitochondrial ROS inhibition prevents doxorubicin-induced breast cancer cell migration and invasion.iScience · 2025Article
- Cancer therapy-related cardiotoxicity is associated with distinct alterations of the myocardial lipidome.European journal of heart failure · 2025Article
- Review
- Cardiomyopathies and a brief insight into DOX-induced cardiomyopathy.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2025Review
- Identifying common pathways for doxorubicin and carfilzomib-induced cardiotoxicities: transcriptomic and epigenetic profiling.Scientific reports · 2025Article
54 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 4 institutions in 1 country.
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Abstract
Doxorubicin (Dox) is a highly effective anticancer drug but cause acute ventricular dysfunction, and also induce late-onset cardiomyopathy and heart failure. Despite extensive studies, the pathogenic sequelae leading to the progression of Dox-associated cardiomyopathy remains unknown. We assessed temporal changes in autophagy, mitochondrial dynamics, and bioenergetics in mouse models of acute and chronic Dox-cardiomyopathy. Time course study of acute Dox-treatment showed accumulation of LC3B II in heart lysates. Autophagy flux assays confirmed that the Dox-induced accumulation of autophagosomes occurs due to blockage of the lysosomal degradation process. Dox-induced autophagosomes and autolysosome accumulation were confirmed in vivo by using GFP-LC3 and mRFP-GFP-LC3 transgenic (Tg) mice. Mitochondria isolated from acute Dox-treated hearts showed significant suppression of oxygen consumption rate (OCR). Chronic Dox-cardiotoxicity also exhibited time-dependent accumulation of LC3B II levels and increased accumulation of green puncta in GFP-LC3 Tg hearts. Mitochondria isolated from chronic Dox-treated hearts also showed significant suppression of mitochondrial OCR. The in vivo impairment of autophagic degradation process and mitochondrial dysfunction data were confirmed in vitro using cultured neonatal cardiomyocytes. Both acute and chronic Dox-associated cardiomyopathy involves a multifocal disease process resulting from autophagosomes and autolysosomes accumulation, altered expression of mitochondrial dynamics and oxidative phosphorylation regulatory proteins, and mitochondrial respiratory dysfunction.
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