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Editorial
. 2023 Apr 28;132(9):1104-1106.
doi: 10.1161/CIRCRESAHA.123.322777. Epub 2023 Apr 27.

Targeting Small-Conductance Calcium-Activated Potassium Channels in Atrial Fibrillation: Therapeutic Opportunities

Xiao-Dong Zhang  1 , Nipavan Chiamvimonvat  1   2   3
Affiliations
Editorial

Targeting Small-Conductance Calcium-Activated Potassium Channels in Atrial Fibrillation: Therapeutic Opportunities

Xiao-Dong Zhang et al. Circ Res. .
No abstract available

Keywords: Editorial; atrial fibrillation; heart; humans; small-conductance calcium-activated potassium channels.

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Conflict of interest statement

Conflict of Interest

The authors declare that there are no conflicts of interest.

Figures

Figure 1.
Figure 1.. SK channels trafficking, gating, and interactome in AF.
SK channels interactome includes α-actinin2 (Actn2), filamin A (FLNA), myosin light chain 2 (MLC2), protein casein kinase II (CK2), protein phosphatase 2A (PP2A). Cardiac SK channels have been shown to couple to L-type Ca2+ channels through a physical bridge, α-actinin2. SK2 channels do not physically interact with the Ca2+ channels, instead the two channels co-localize via their interaction with α-actinin2 along the Z-line in atrial myocytes. AF or tachypacing, may not alter the expression of SK channels in atrial myocytes, but increase calmodulin (CaM) expression, enhance association of α-actinin2 with SK channels, increase dephosphorylation of CaM by PP2A, and stimulate SK channel forward trafficking and membrane targeting. This results in increased SK currents, shortening of the atrial action potentials, and maintenance of arrhythmias. Schematic representation was generated using BioRender.
See this image and copyright information in PMC

Comment on

References

    1. Xu Y, Tuteja D, Zhang Z, Xu D, Zhang Y, Rodriguez J, Nie L, Tuxson HR, Young JN, Glatter KA, et al.. Molecular identification and functional roles of a Ca2+-activated K+ channel in human and mouse hearts. J Biol Chem. 2003;278:49085–49094 - PubMed
    1. Zhang Q, Timofeyev V, Lu L, Li N, Singapuri A, Long MK, Bond CT, Adelman JP, Chiamvimonvat N. Functional roles of a Ca2+-activated K+ channel in atrioventricular nodes. Circ Res. 2008;102:465–471 - PMC - PubMed
    1. Torrente AG, Zhang R, Wang H, Zaini A, Kim B, Yue X, Philipson KD, Goldhaber JI. Contribution of small conductance K+ channels to sinoatrial node pacemaker activity: Insights from atrial-specific Na+/Ca2+ exchange knockout mice. J Physiol. 2017;595:3847–3865 - PMC - PubMed
    1. Zhang XD, Lieu DK, Chiamvimonvat N. Small-conductance Ca2+-activated K+ channels and cardiac arrhythmias. Heart Rhythm. 2015;12:1845–1851 - PMC - PubMed
    1. Zhang XD, Thai PN, Lieu DK, Chiamvimonvat N. Cardiac small-conductance calcium-activated potassium channels in health and disease. Pflugers Arch. 2021;473:477–489 - PMC - PubMed

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