ArticleBritish journal of pharmacology2018
Quantifying the relationship between inhibition of VEGF receptor 2, drug-induced blood pressure elevation and hypertension.
Article in British journal of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 20 citations in OpenAlex.
- Losartan Alleviates the Side Effects and Maintains the Anticancer Activity of Axitinib.Molecules (Basel, Switzerland) · 2022Article
- The vascular endothelial growth factor trap aflibercept induces vascular dysfunction and hypertension via attenuation of eNOS/NO signaling in mice.Acta pharmacologica Sinica · 2021Article
- Design and optimisation of dendrimer-conjugated Bcl-2/xCommunications biology · 2021Article
- Precision Cardio-Oncology: Use of Mechanistic Pharmacokinetic and Pharmacodynamic Modeling to Predict Cardiotoxicities of Anti-Cancer Drugs.Frontiers in oncology · 2021Review
- Long-term cardiovascular effects of vandetanib and pazopanib in normotensive rats.Pharmacology research & perspectives · 2019Article
- Peptide P7 inhibits the bFGF-stimulated proliferation and invasion of SKOV3 cells.Experimental and therapeutic medicine · 2019Article
- Quantifying the relationship between inhibition of VEGF receptor 2, drug-induced blood pressure elevation and hypertension.British journal of pharmacology · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeSeveral anti-angiogenic cancer drugs that inhibit VEGF receptor (VEGFR) signalling for efficacy are associated with a 15-60% incidence of hypertension. Tyrosine kinase inhibitors (TKIs) that have off-target activity at VEGFR-2 may also cause blood pressure elevation as an undesirable side effect. Therefore, the ability to translate VEGFR-2 off-target potency into blood pressure elevation would be useful in development of novel TKIs. Here, we have sought to quantify the relationship between VEGFR-2 inhibition and blood pressure elevation for a range of kinase inhibitors. EXPERIMENTAL APPROACH: Porcine aortic endothelial cells overexpressing VEGFR-2 (PAE) were used to determine IC KEY
resultsAll-grade hypertension was predominantly observed when the C CONCLUSIONS AND IMPLICATIONS: Taken together, these data show that the risk of blood pressure elevation is proportional to the amount of VEGFR-2 inhibition, and a margin of >10-fold between VEGFR-2 IC
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