ArticlePloS one2013
The Ca²⁺-activated K⁺ channel KCa3.1 as a potential new target for the prevention of allograft vasculopathy.
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 14 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- The KCa3.1 KCells · 2026Review
- Efficacy of combined tumor irradiation and KScientific reports · 2023Article
- Muscle Damage in Dystrophic mdx Mice Is Influenced by the Activity of CaLife (Basel, Switzerland) · 2022Article
- Midazolam's Effects on Delayed-Rectifier KInternational journal of molecular sciences · 2021Article
- Pharmacology of Small- and Intermediate-Conductance Calcium-Activated Potassium Channels.Annual review of pharmacology and toxicology · 2020Review
- Inhibition of the potassium channel Kv1.3 reduces infarction and inflammation in ischemic stroke.Annals of clinical and translational neurology · 2018Article
- KCa3.1 Channel Modulators as Potential Therapeutic Compounds for Glioblastoma.Current neuropharmacology · 2018Article
- Structural Insights into the Atomistic Mechanisms of Action of Small Molecule Inhibitors Targeting the KCa3.1 Channel Pore.Molecular pharmacology · 2017Article
- Potassium Channels in Regulation of Vascular Smooth Muscle Contraction and Growth.Advances in pharmacology (San Diego, Calif.) · 2017Review
- The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016Article
- Protein transduction therapy into cochleae via the round window niche in guinea pigs.Molecular therapy. Methods & clinical development · 2016Article
- Ion channels in innate and adaptive immunity.Annual review of immunology · 2015Review
- NMDA-receptor antagonists block B-cell function but foster IL-10 production in BCR/CD40-activated B cells.Cell communication and signaling : CCS · 2014Article
- Modulation of K(Ca)3.1 channels by eicosanoids, omega-3 fatty acids, and molecular determinants.PloS one · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Allograft vasculopathy (AV) remains one of the major challenges to the long-term functioning of solid organ transplants. Although its exact pathogenesis remains unclear, AV is characterized by both fibromuscular proliferation and infiltration of CD4(+) memory T cells. We here tested whether two experimental immunosuppressants targeting K(+) channels might be useful for preventing AV. PAP-1 inhibits the voltage-gated Kv1.3 channel, which is overexpressed on CCR7(-) memory T cells and we therefore hypothesize that it should suppress the memory T cell component of AV. Based on its previous efficacy in restenosis and kidney fibrosis we expected that the KCa3.1 blocker TRAM-34 would primarily affect smooth muscle and fibroblast proliferation and thus reduce intimal hyperplasia. Using immunohistochemistry we demonstrated the presence of Kv1.3 on infiltrating T cells and of KCa3.1 on lymphocytes as well as on proliferating neointimal smooth muscle cells in human vasculopathy samples and in a rat aorta transplant model developing chronic AV. Treatment of PVG rats receiving orthotopically transplanted aortas from ACI rats with TRAM-34 dose-dependently reduced aortic luminal occlusion, intimal hyperplasia, mononuclear cell infiltration and collagen deposition 120 days after transplantation. The Kv1.3 blocker PAP-1 in contrast did not reduce intima hyperplasia despite drastically reducing plasma IFN-γ levels and inhibiting lymphocyte infiltration. Our findings suggest that KCa3.1 channels play an important role in the pathogenesis of chronic AV and constitute an attractive target for the prevention of arteriopathy.
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Registered trials
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