ArticleCardiovascular research2011
Potent suppression of vascular smooth muscle cell migration and human neointimal hyperplasia by KV1.3 channel blockers.
Article in Cardiovascular research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 59 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
- Effects of β-adrenoceptor antagonist and 5-HTThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
- Vascular Smooth Muscle Cell Migration and P70S6K: Key Players in Intimal Hyperplasia Development.Journal of the American Heart Association · 2025Article
- A sex-dependent role of Kv1.3 channels from macrophages in metabolic syndrome.Frontiers in physiology · 2024Article
- Simvastatin and dehydroepiandrosterone sulfate effects against hypoxic pulmonary hypertension are not additive.Physiological research · 2022Article
- Review
- Large-conductance CaFrontiers in cardiovascular medicine · 2022Article
- Kv1.3 voltage-gated potassium channels link cellular respiration to proliferation through a non-conducting mechanism.Cell death & disease · 2021Article
- The role of P2Y12 receptor inhibition in ischemic stroke on microglia, platelets and vascular smooth muscle cells.Journal of thrombosis and thrombolysis · 2020Review
- Contribution of the Potassium Channels KCells · 2020Article
- Blockage of Kv1.3 regulates macrophage migration in acute liver injury by targeting δ-catenin through RhoA signaling.International journal of biological sciences · 2020Article
- Voltage-Gated Potassium Channels as Regulators of Cell Death.Frontiers in cell and developmental biology · 2020Review
- Myocardin and Kv1 Channels: A Paradigm Shift in Treating Vascular Smooth Muscle Cell-Related Proliferative Disease?Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Kv1.3 activity perturbs the homeostatic properties of astrocytes in glioma.Scientific reports · 2018Article
- Diabetes Mellitus and Ischemic Heart Disease: The Role of Ion Channels.International journal of molecular sciences · 2018Review
- Angiotensin II reduces the surface abundance of KThe Journal of physiology · 2017Article
- Potassium Channels in Regulation of Vascular Smooth Muscle Contraction and Growth.Advances in pharmacology (San Diego, Calif.) · 2017Review
- Intravascular pressure enhances the abundance of functional Kv1.5 channels at the surface of arterial smooth muscle cells.Science signaling · 2015Article
- Endogenous animal toxin-like human β-defensin 2 inhibits own K(+) channels through interaction with channel extracellular pore region.Cellular and molecular life sciences : CMLS · 2015Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
aimThe aim of the study was to determine the potential for K(V)1 potassium channel blockers as inhibitors of human neoinitimal hyperplasia. METHODS AND
resultsBlood vessels were obtained from patients or mice and studied in culture. Reverse transcriptase-polymerase chain reaction and immunocytochemistry were used to detect gene expression. Whole-cell patch-clamp, intracellular calcium measurement, cell migration assays, and organ culture were used to assess channel function. K(V)1.3 was unique among the K(V)1 channels in showing preserved and up-regulated expression when the vascular smooth muscle cells switched to the proliferating phenotype. There was strong expression in neointimal formations. Voltage-dependent potassium current in proliferating cells was sensitive to three different blockers of K(V)1.3 channels. Calcium entry was also inhibited. All three blockers reduced vascular smooth muscle cell migration and the effects were non-additive. One of the blockers (margatoxin) was highly potent, suppressing cell migration with an IC(50) of 85 pM. Two of the blockers were tested in organ-cultured human vein samples and both inhibited neointimal hyperplasia.
conclusionK(V)1.3 potassium channels are functional in proliferating mouse and human vascular smooth muscle cells and have positive effects on cell migration. Blockers of the channels may be useful as inhibitors of neointimal hyperplasia and other unwanted vascular remodelling events.
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Registered trials
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.