ArticleFrontiers in physiology2018
Rho-Kinase Inhibition Ameliorates Dasatinib-Induced Endothelial Dysfunction and Pulmonary Hypertension.
Article in Frontiers in physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Drug-induced pulmonary edema: a real-world pharmacovigilance study using the FDA Adverse Event Reporting System (FAERS).Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025Article
- Endothelium as a Source of Cardiovascular Toxicity From Antitumor Kinase Inhibitors.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- A Comprehensive Review of Cancer Drug-Induced Cardiotoxicity in Blood Cancer Patients: Current Perspectives and Therapeutic Strategies.Current treatment options in oncology · 2024Review
- Pentastatin, a matrikine of the collagen IVα5, is a novel endogenous mediator of pulmonary endothelial dysfunction.American journal of physiology. Cell physiology · 2023Article
- Imatinib attenuates reperfusion injury in a rat model of acute myocardial infarction.Basic research in cardiology · 2023Article
- Adverse reactions after treatment with dasatinib in chronic myeloid leukemia: Characteristics, potential mechanisms, and clinical management strategies.Frontiers in oncology · 2023Review
- Differential Expression Profile of microRNAs and Tight Junction in the Lung Tissues of Rat With Mitomycin-C-Induced Pulmonary Veno-Occlusive Disease.Frontiers in cardiovascular medicine · 2022Article
- Melatonin Attenuates Dasatinib-Aggravated Hypoxic Pulmonary Hypertension via Inhibiting Pulmonary Vascular Remodeling.Frontiers in cardiovascular medicine · 2022Article
- A narrative review on adverse effects of dasatinib with a focus on pharmacotherapy of dasatinib-induced pulmonary toxicities.Blood research · 2021Review
- Exploiting polypharmacology to dissect host kinases and kinase inhibitors that modulate endothelial barrier integrity.Cell chemical biology · 2021Article
- Inhibition of Rho-kinase is involved in the therapeutic effects of atorvastatin in heart ischemia/reperfusion.Experimental and therapeutic medicine · 2020Article
- Mechanisms of Cardiovascular Toxicity of BCR-ABL1 Tyrosine Kinase Inhibitors in Chronic Myelogenous Leukemia.Current hematologic malignancy reports · 2020Review
- Tyrosine Kinase Inhibitors in Leukemia and Cardiovascular Events: From Mechanism to Patient Care.Arteriosclerosis, thrombosis, and vascular biology · 2020Review
- EXPRESS: Pulmonary hypertension with dasatinib and other tyrosine kinase inhibitors.Pulmonary circulation · 2019Article
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The multi-kinase inhibitor dasatinib is used for treatment of imatinib-resistant chronic myeloid leukemia, but is prone to induce microvascular dysfunction. In lung this can manifest as capillary leakage with pleural effusion, pulmonary edema or even pulmonary arterial hypertension. To understand how dasatinib causes endothelial dysfunction we examined the effects of clinically relevant concentrations of dasatinib on both human pulmonary arterial macro- and microvascular endothelial cells (ECs). The effects of dasatinib was compared to imatinib and nilotinib, two other clinically used BCR/Abl kinase inhibitors that do not inhibit Src. Real three-dimensional morphology and high resolution stiffness mapping revealed softening of both macro- and microvascular ECs upon dasatinib treatment, which was not observed in response to imatinib. In a dose-dependent manner, dasatinib decreased transendothelial electrical resistance/impedance and caused a permeability increase as well as disruption of tight adherens junctions in both cell types. In isolated perfused and ventilated rat lungs, dasatinib increased mean pulmonary arterial pressure, which was accompanied by a gain in lung weight. The Rho-kinase inhibitor Y27632 partly reversed the dasatinib-induced changes
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