ArticleCardiovascular research2023
Doxorubicin-induced cardiovascular toxicity: a longitudinal evaluation of functional and molecular markers.
Article in Cardiovascular research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Cardiovascular Protection with Sulfasalazine During Doxorubicin Challenge: Evidence from Oxidative and Histologic Endpoints.Biomolecules · 2026Article
- Modulation of the ACLY-AMPK axis by bempedoic acid suppresses NF-κB-driven inflammation, VEGF-Notch angiogenic crosstalk, and cell-cycle progression in Solid Ehrlich Carcinoma.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Neuregulin-1β Mitigates Doxorubicin-Induced Cardiotoxicity viaInternational journal of molecular sciences · 2026Article
- Article
- Cysteine imaging reveals early redox dysregulation and identifies gnetol as a ferroptosis-modulating agent in doxorubicin cardiotoxicity.Redox biology · 2026Article
- TAX1BP1 protects against doxorubicin-induced cardiotoxicity via maintaining mitochondrial function in a mTORC2-SGK1-VDAC1 manner.Molecular medicine (Cambridge, Mass.) · 2026Article
- Integrated Omics Approach to Delineate the Mechanisms of Doxorubicin-Induced Cardiotoxicity.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Mesenchymal Stem Cells Membrane Biomimetic Nanoplatform for Glioblastoma-Targeted Combinatorial Chemotherapy.International journal of nanomedicine · 2026Article
- Sustained mesenchymal reprogramming of endothelial cells after completion of chemotherapy.Cardio-oncology (London, England) · 2025Article
- THBS1BMC medicine · 2025Article
- Redox-Responsive π-Conjugated Prodrug Nanoassemblies for Cancer Chemotherapy.Pharmaceutics · 2025Article
- MICRORNA-146B TARGETS HIF-1Α AND ATTENUATES CARDIOMYOCYTE APOPTOSIS AND FIBROSIS IN DOXORUBICIN-INDUCED HEART FAILURE.Shock (Augusta, Ga.) · 2025Article
- Dynamics of SERPINA3 in response to anthracycline treatment and cardiovascular dysfunction.Cardio-oncology (London, England) · 2025Article
- Distinct Impact of Doxorubicin on Skeletal Muscle and Fat Metabolism in Mice: Without Dexrazoxane Effect.International journal of molecular sciences · 2025Article
- Intravenous Thrombolysis for Pediatric Ischemic Stroke Secondary to Cancer Therapy-related Cardiac Dysfunction.Internal medicine (Tokyo, Japan) · 2025Article
- Cardioprotective effect ofActa biochimica et biophysica Sinica · 2024Article
- Article
- Dexrazoxane prevents vascular toxicity in doxorubicin-treated mice.Cardio-oncology (London, England) · 2024Article
- Characterization of systolic and diastolic function, alongside proteomic profiling, in doxorubicin-induced cardiovascular toxicity in mice.Cardio-oncology (London, England) · 2024Article
- 4-Deoxy-Drug design, development and therapy · 2024Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
aimsApart from cardiotoxicity, the chemotherapeutic doxorubicin (DOX) induces vascular toxicity, represented by arterial stiffness and endothelial dysfunction. Both parameters are of interest for cardiovascular risk stratification as they are independent predictors of future cardiovascular events in the general population. However, the time course of DOX-induced cardiovascular toxicity remains unclear. Moreover, current biomarkers for cardiovascular toxicity prove insufficient. Here, we longitudinally evaluated functional and molecular markers of DOX-induced cardiovascular toxicity in a murine model. Molecular markers were further validated in patient plasma. METHODS AND
resultsDOX (4 mg/kg) or saline (vehicle) was administered intra-peritoneally to young, male mice weekly for 6 weeks. In vivo cardiovascular function and ex vivo arterial stiffness and vascular reactivity were evaluated at baseline, during DOX therapy (Weeks 2 and 4) and after therapy cessation (Weeks 6, 9, and 15). Left ventricular ejection fraction (LVEF) declined from Week 4 in the DOX group. DOX increased arterial stiffness in vivo and ex vivo at Week 2, which reverted thereafter. Importantly, DOX-induced arterial stiffness preceded reduced LVEF. Further, DOX impaired endothelium-dependent vasodilation at Weeks 2 and 6, which recovered at Weeks 9 and 15. Conversely, contraction with phenylephrine was consistently higher in the DOX-treated group. Furthermore, proteomic analysis on aortic tissue identified increased thrombospondin-1 (THBS1) and alpha-1-antichymotrypsin (SERPINA3) at Weeks 2 and 6. Up-regulated THBS1 and SERPINA3 persisted during follow-up. Finally, THBS1 and SERPINA3 were quantified in plasma of patients. Cancer survivors with anthracycline-induced cardiotoxicity (AICT; LVEF < 50%) showed elevated THBS1 and SERPINA3 levels compared with age-matched control patients (LVEF ≥ 60%).
conclusionsDOX increased arterial stiffness and impaired endothelial function, which both preceded reduced LVEF. Vascular dysfunction restored after DOX therapy cessation, whereas cardiac dysfunction persisted. Further, we identified SERPINA3 and THBS1 as promising biomarkers of DOX-induced cardiovascular toxicity, which were confirmed in AICT patients.
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