ArticleFrontiers in pharmacology2020
Exploration the Mechanism of Doxorubicin-Induced Heart Failure in Rats by Integration of Proteomics and Metabolomics Data.
Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- A narrative review of metabolomics approaches in identifying biomarkers of doxorubicin-induced cardiotoxicity.Metabolomics : Official journal of the Metabolomic Society · 2025Pooled it
- Anthracycline-induced cardiotoxicity associated with myocardial energy metabolism: mechanisms revealed through an integration ofFrontiers in cardiovascular medicine · 2025Trial
- Early cardiac proteomic profiling in a long-latency doxorubicin cardiomyopathy model exhibits sexual dimorphism for cardioprotection.Journal of molecular and cellular cardiology plus · 2026Article
- Control of cardiotoxicity via nasal in-situ pH-sensitive transbilosomal formulation of candesartan.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- SWATH-MS for discovery of early biomarkers of drug-induced cardiotoxicity using an animal doxorubicin model.Cardio-oncology (London, England) · 2026Article
- In vivo dynamic nuclear polarization magnetic resonance imaging reveals cardiac mitochondrial redox imbalance as an early indicator of heart failure.Redox biology · 2026Article
- [3-Npj imaging · 2026Article
- Cross-modal integration of metabolomics and cardiac functionality captures dynamic metabotoxic effects of doxorubicin in engineered heart tissues.Stem cell reports · 2026Article
- Effects of dietary supplementation with astragalus polysaccharides on growth performance, serum parameters, and rumen microbial function of yaks.BMC microbiology · 2025Article
- Astragaloside IV ameliorates cardiomyocyte injury and heart failure through hif/rho/rock pathway regulation: In vitro and in vivo insights.Journal of bioenergetics and biomembranes · 2025Article
- DNA-damage-associated protein co-expression network in cardiomyocytes informs on tolerance to genetic variation and disease.iScience · 2025Article
- SNP's use as a potential chemotoxicity stratification tool in breast cancer: from bench to clinic.Functional & integrative genomics · 2025Review
- Methodological Aspects of μLC-MS/MS for Wide-Scale Proteomic Analysis of Anthracycline-Induced Cardiomyopathy.ACS omega · 2025Article
- Small Extracellular Vesicles from Breast Cancer Cells Induce Cardiotoxicity.International journal of molecular sciences · 2025Article
- Molecular and metabolic landscape of adenosine triphosphate-induced cell death in cardiovascular disease.World journal of cardiology · 2024Review
- Genetic factors in the pathogenesis of cardio-oncology.Journal of translational medicine · 2024Review
- Computational approaches identify a transcriptomic fingerprint of drug-induced structural cardiotoxicity.Cell biology and toxicology · 2024Article
- Characterization of systolic and diastolic function, alongside proteomic profiling, in doxorubicin-induced cardiovascular toxicity in mice.Cardio-oncology (London, England) · 2024Article
- Precision Cardio-oncology: Update on Omics-Based Diagnostic Methods.Current treatment options in oncology · 2024Review
- Water Extract ofInternational journal of molecular sciences · 2023Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heart failure is a common systemic disease with high morbidity and mortality worldwide. Doxorubicin (DOX) is a commonly used anthracycline broad-spectrum antitumor antibiotic with strong antitumor effect and definite curative effect. However, cardiotoxicity is the adverse reaction of drug dose cumulative toxicity, but the mechanism is still unclear. In this study, proteomics and metabonomics techniques were used to analyze the tissue and plasma of DOX-induced heart failure (HF) in rats and to clarify the molecular mechanism of the harmful effects of DOX on cardiac metabolism and function in rats from a new point of view. The results showed that a total of 278 proteins with significant changes were identified by quantitative proteomic analysis, of which 118 proteins were significantly upregulated and 160 proteins were significantly downregulated in myocardial tissue. In the metabonomic analysis, 21 biomarkers such as L-octanoylcarnitine, alpha-ketoglutarate, glutamine, creatine, and sphingosine were detected. Correlation analysis showed that DOX-induced HF mainly affected phenylalanine, tyrosine, and tryptophan biosynthesis, D-glutamine and D-glutamate metabolism, phenylalanine metabolism, biosynthesis of unsaturated fatty acids, and other metabolic pathways, suggesting abnormal amino acid metabolism, fatty acid metabolism, and glycerol phospholipid metabolism. It is worth noting that we have found the key upstream target of DOX-induced HF, PTP1B, which inhibits the expression of HIF-1α by inhibiting the phosphorylation of IRS, leading to disorders of fatty acid metabolism and glycolysis, which together with the decrease of Nrf2, SOD, Cytc, and AK4 proteins lead to oxidative stress. Therefore, we think that PTP1B may play an important role in the development of heart failure induced by doxorubicin and can be used as a potential target for the treatment of heart failure.
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