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Title: The K+ channels KCa3.1 and Kv1.3 as novel targets for asthma therapy
Authors: Bradding, Peter
Wulff, Heike
First Published: 29-Jul-2003
Publisher: Wiley-Blackwell on behalf of The British Pharmacological Society
Citation: British Journal of Pharmacology, 2009, 157 (8), pp. 1330-1339
Abstract: Asthma affects 10% of the UK population and is an important cause of morbidity and mortality at all ages. Current treatments are either ineffective or carry unacceptable side effects for a number of patients; in consequence, development of new approaches to therapy are important. Ion channels are emerging as attractive therapeutic targets in a variety of non-excitable cells. Ion channels conducting K+ modulate the activity of several structural and inflammatory cells which play important roles in the pathophysiology of asthma. Two channels of particular interest are the voltage-gated K+ channel Kv1.3 and the intermediate conductance Ca2+-activated K+ channel KCa3.1 (also known as IKCa1 or SK4). Kv1.3 is expressed in IFNγ-producing T cells while KCa3.1 is expressed in T cells, mast cells, macrophages, airway smooth muscle cells, fibroblasts and epithelial cells. Both channels play important roles in cell activation, migration and proliferation through the regulation of membrane potential and calcium signalling. We hypothesise that KCa3.1- and/or Kv1.3-dependent cell processes are one of the common denominators in asthma pathophysiology. If true, these channels might serve as novel targets for the treatment of asthma. Emerging evidence lends support to this hypothesis. Further validation through the study of the role these channels play in normal and asthmatic airway cell (patho)physiology and in vivo models will provide further justification for the assessment of small molecule blockers of Kv1.3 and KCa3.1 in the treatment of asthma.
DOI Link: 10.1111/j.1476-5381.2009.00362.x
ISSN: 0007-1188
Type: Article
Rights: This is the author’s final draft of the paper published as British Journal of Pharmacology, 2009, 157 (8), pp. 1330-1339 . The final published version is available at, Doi: 10.1111/j.1476-5381.2009.00362.x.
Appears in Collections:Published Articles, Dept. of Infection, Immunity and Inflammation

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