ArticlePloS one2013
Doxorubicin-induced vascular toxicity--targeting potential pathways may reduce procoagulant activity.
Article in PloS one, 2013. 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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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.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- ADAMTS13 as a thromboinflammatory brake at the vascular-immune interface: from viral immunothrombosis to the tumor microenvironment.Frontiers in immunology · 2026Review
- From signal to significance: characterizing anthracycline-related hypercoagulable adverse events via pharmacovigilance, animal models, and clinical observation.Frontiers in pharmacology · 2026Article
- Article
- Recent Advances in the Mechanisms of Cell Death and Dysfunction in Doxorubicin Cardiotoxicity.Reviews in cardiovascular medicine · 2023Review
- Revisiting treatment-related cardiotoxicity in patients with malignant lymphoma-a review and prospects for the future.Frontiers in cardiovascular medicine · 2023Review
- Doxorubicin-Induced Platelet Activation and Clearance Relieved by Salvianolic Acid Compound: Novel Mechanism and Potential Therapy for Chemotherapy-Associated Thrombosis and Thrombocytopenia.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Coronary microcirculation damage in anthracycline cardiotoxicity.Cardiovascular research · 2022Article
- Irinotecan (CPT-11) Treatment Induces Mild Gonadotoxicity.Frontiers in reproductive health · 2022Article
- Chemotherapy-induced acute vascular injury involves intracellular generation of ROS via activation of the acid sphingomyelinase pathway.Cellular signalling · 2021Article
- Cancer Therapy-Associated Thrombosis.Arteriosclerosis, thrombosis, and vascular biology · 2021Review
- Novel Mechanisms of Anthracycline-Induced Cardiovascular Toxicity: A Focus on Thrombosis, Cardiac Atrophy, and Programmed Cell Death.Frontiers in cardiovascular medicine · 2021Review
- Anti-HER2/neu Antibody Reduces Chemotherapy-Induced Ovarian Toxicity-From Bench to Bedside.Biomedicines · 2020Article
- Cancer During Pregnancy: The Role of Vascular Toxicity in Chemotherapy-Induced Placental Toxicity.Cancers · 2020Article
- Article
- Cardiotoxic Profile and Arterial Stiffness of Adjuvant Chemotherapy for Colorectal Cancer.Cancer management and research · 2020Article
- Anti-cancer drugs-induced arterial injury: risk stratification, prevention, and treatment.Medical oncology (Northwood, London, England) · 2019Review
- Study on the infusion-site adverse events and vascular distribution of epirubicin in chemotherapy with epirubicin and fosaprepitant.Molecular and clinical oncology · 2019Article
- Arterial stiffness in hematologic malignancies.OncoTargets and therapy · 2017Review
- The interplay between genetic background and sexual dimorphism of doxorubicin-induced cardiotoxicity.Cardio-oncology (London, England) · 2016Article
- Long-Term Follow-Up of Chemotherapy-Induced Ovarian Failure in Young Breast Cancer Patients: The Role of Vascular Toxicity.The oncologist · 2015Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionPrevious study in mice using real-time intravital imaging revealed an acute deleterious effect of doxorubicin (DXR) on the gonadal vasculature, as a prototype of an end-organ, manifested by a reduction in blood flow and disintegration of the vessel wall. We hypothesized that this pattern may represent the formation of microthrombi. We aimed to further characterize the effect of DXR on platelets' activity and interaction with endothelial cells (EC) and to examine potential protectants to reduce DXR acute effect on the blood flow.
methodsThe effect of DXR on platelet adhesion and aggregation were studied in vitro. For in vivo studies, mice were injected with either low molecular weight heparin (LMWH; Enoxaparin) or with eptifibatide (Integrilin(©)) prior to DXR treatment. Testicular arterial blood flow was examined in real-time by pulse wave Doppler ultrasound.
resultsPlatelet treatment with DXR did not affect platelet adhesion to a thrombogenic surface but significantly decreased ADP-induced platelet aggregation by up to 40% (p<0.001). However, there was a significant increase in GPIIbIIIa-mediated platelet adhesion to DXR-exposed endothelial cells (EC; 5.7-fold; p<0.001) reflecting the toxic effect of DXR on EC. The testicular arterial blood flow was preserved in mice pre-treated with LMWH or eptifibatide prior to DXR (P<0.01).
conclusionsDXR-induced acute vascular toxicity may involve increased platelet-EC adhesion leading to EC-bound microthrombi formation resulting in compromised blood flow. Anti-platelet/anti-coagulant agents are effective in reducing the detrimental effect of DXR on the vasculature and thus may serve as potential protectants to lessen this critical toxicity.
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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.