Kv7 Channels and Excitability Disorders
- PMID: 33860384
- DOI: 10.1007/164_2021_457
Kv7 Channels and Excitability Disorders
Abstract
Kv7.1-Kv7.5 (KCNQ1-5) K+ channels are voltage-gated K+ channels with major roles in neurons, muscle cells and epithelia where they underlie physiologically important K+ currents, such as neuronal M current and cardiac IKs. Specific biophysical properties of Kv7 channels make them particularly well placed to control the activity of excitable cells. Indeed, these channels often work as 'excitability breaks' and are targeted by various hormones and modulators to regulate cellular activity outputs. Genetic deficiencies in all five KCNQ genes result in human excitability disorders, including epilepsy, arrhythmias, deafness and some others. Not surprisingly, this channel family attracts considerable attention as potential drug targets. Here we will review biophysical properties and tissue expression profile of Kv7 channels, discuss recent advances in the understanding of their structure as well as their role in various neurological, cardiovascular and other diseases and pathologies. We will also consider a scope for therapeutic targeting of Kv7 channels for treatment of the above health conditions.
Keywords: Channelopathy; Epilepsy; KCNQ; Kv7 channel; M current; Pain.
© 2021. The Author(s), under exclusive license to Springer Nature Switzerland AG.
Similar articles
-
The therapeutic potential of neuronal KCNQ channel modulators.Expert Opin Ther Targets. 2003 Dec;7(6):737-48. doi: 10.1517/14728222.7.6.737. Expert Opin Ther Targets. 2003. PMID: 14640909 Review.
-
Kv7 channels as targets for the treatment of pain.Curr Pharm Des. 2009;15(15):1773-98. doi: 10.2174/138161209788186326. Curr Pharm Des. 2009. PMID: 19442190 Review.
-
Electrophysiological and pharmacological characterization of a novel and potent neuronal Kv7 channel opener SCR2682 for antiepilepsy.FASEB J. 2019 Aug;33(8):9154-9166. doi: 10.1096/fj.201802848RR. Epub 2019 May 7. FASEB J. 2019. PMID: 31063701
-
Activation of Kv7 (KCNQ) voltage-gated potassium channels by synthetic compounds.Trends Pharmacol Sci. 2008 Feb;29(2):99-107. doi: 10.1016/j.tips.2007.11.010. Epub 2008 Jan 18. Trends Pharmacol Sci. 2008. PMID: 18206251 Review.
-
HCN and KV7 (M-) channels as targets for epilepsy treatment.Neuropharmacology. 2013 Jun;69:75-81. doi: 10.1016/j.neuropharm.2012.03.005. Epub 2012 Mar 15. Neuropharmacology. 2013. PMID: 22446478 Free PMC article. Review.
Cited by
-
Circuit-based intervention corrects excessive dentate gyrus output in the Fragile X mouse model.bioRxiv [Preprint]. 2023 Nov 13:2023.09.27.559792. doi: 10.1101/2023.09.27.559792. bioRxiv. 2023. Update in: Elife. 2024 Feb 12;12:RP92563. doi: 10.7554/eLife.92563. PMID: 37808793 Free PMC article. Updated. Preprint.
-
A novel dual serotonin transporter and M-channel inhibitor D01 for antidepression and cognitive improvement.Acta Pharm Sin B. 2024 Mar;14(3):1457-1466. doi: 10.1016/j.apsb.2023.11.024. Epub 2023 Nov 24. Acta Pharm Sin B. 2024. PMID: 38487010 Free PMC article.
-
Evidence for Dual Activation of IK(M) and IK(Ca) Caused by QO-58 (5-(2,6-Dichloro-5-fluoropyridin-3-yl)-3-phenyl-2-(trifluoromethyl)-1H-pyrazolol[1,5-a]pyrimidin-7-one).Int J Mol Sci. 2022 Jun 24;23(13):7042. doi: 10.3390/ijms23137042. Int J Mol Sci. 2022. PMID: 35806047 Free PMC article.
-
Circuit-based intervention corrects excessive dentate gyrus output in the fragile X mouse model.Elife. 2024 Feb 12;12:RP92563. doi: 10.7554/eLife.92563. Elife. 2024. PMID: 38345852 Free PMC article.
-
Neuropathic pain; what we know and what we should do about it.Front Pain Res (Lausanne). 2023 Sep 22;4:1220034. doi: 10.3389/fpain.2023.1220034. eCollection 2023. Front Pain Res (Lausanne). 2023. PMID: 37810432 Free PMC article. Review.
References
-
- Adduci A, Martire M, Taglialatela M, Arena V, Rizzo G, Coco C, Currò D (2013) Expression and motor functional roles of voltage-dependent type 7 K(+) channels in the human taenia coli. Eur J Pharmacol 721:12–20 - PubMed
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
Molecular Biology Databases