ArticleTurkish journal of pharmaceutical sciences2019
Anti-Angiogenic Activity of Flunarizine by
Article in Turkish journal of pharmaceutical sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed, 6 citations in OpenAlex.
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- Extracorporeal Shock Wave Therapy Salvages Critical Limb Ischemia in B6 Mice through Upregulating Cell Proliferation Signaling and Angiogenesis.Biomedicines · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesThe involvement of T-type calcium channels in cell proliferation and the role of sodium channels in cell migration have been extensively studied in angiogenesis. In the present study, flunarizine, a dual sodium/calcium channel blocker; was selected to evaluate its anti-angiogenic potential. This can be therapeutically beneficial in diseases caused by pathologically excessive angiogenesis. MATERIALS AND
methodsThe anti-angiogenic activity of ion channel blocker was screened by chick chorioallantoic membrane assay
resultsAll the groups were compared with the control group using one-way ANOVA, followed by a post hoc test, Dunnett's test, to compare the mean of all the groups with the control mean. In the chick chorioallantoic membrane assay, the number of branching points and angiogenic score were evaluated and significant results were observed at 10
conclusionFlunarizine has significant anti-angiogenic action by inhibiting cell proliferation, migration, and cord-like tube formation, which resulted from blocking of the T-type calcium and sodium channels. Further studies on the structural modifications of flunarizine for repurposing this ion channel modulator will lead to treatment of the diseases due to excessive angiogenesis from the root cause.
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Registered trials
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