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The role of connexin-43 in modeling arrhythmogenic diseases with induced pluripotent stem cell-derived cardiomyocytes

A common pathophysiological characteristic of arrhythmic diseases is the disruption of electrical signal transmission across the heart causing life-threatening rhythm disorders. These conditions are associated with decreased expression of connexin-43 (Cx43) at intercalated discs and its translocatio...

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Main Authors: Ke, Xijian (Author) , Baillie, Jonathan S. (Author) , Lemma, Enrico D. (Author) , Bastmeyer, Martin (Author) , Hecker, Markus (Author) , Ullrich, Nina D. (Author)
Format: Article (Journal)
Language:English
Published: July 2025
In: Journal of molecular and cellular cardiology
Year: 2025, Volume: 204, Pages: 79-88
ISSN:1095-8584
DOI:10.1016/j.yjmcc.2025.05.008
Online Access:Verlag, kostenfrei, Volltext: https://doi.org/10.1016/j.yjmcc.2025.05.008
Verlag, kostenfrei, Volltext: https://www.sciencedirect.com/science/article/pii/S0022282825000902
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Author Notes:Xijian Ke, Jonathan S. Baillie, Enrico D. Lemma, Martin Bastmeyer, Markus Hecker, Nina D. Ullrich
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Summary:A common pathophysiological characteristic of arrhythmic diseases is the disruption of electrical signal transmission across the heart causing life-threatening rhythm disorders. These conditions are associated with decreased expression of connexin-43 (Cx43) at intercalated discs and its translocation to the lateral membranes, however, the underlying mechanisms remain unclear. Induced pluripotent stem cell-derived cardiomyocytes (iPSC-CM) offer a model for studying these pathophysiological processes. Here, we tested the hypothesis that chronic stress, usually preceding arrhythmic developments, modulates Cx43 expression. iPSC-CM were electrically stimulated at a normal rate and by tachypacing, and their electrical and Ca2+ signaling properties were analyzed. Our data revealed that tachypacing significantly reduced Cx43 expression by a micro-RNA miR-1-dependent mechanism. Anti-miR-1 treatment restored Cx43 expression in conditions of stress, enhanced Na+ currents, improved Ca2+ propagation and synchronized electrical activity. These findings suggest miR-1 as a potential pharmacological target for mitigating arrhythmogenic remodeling and restoring robust electrical signal transmission in cardiomyocytes.
Item Description:Online verfügbar: 26. Mai 2025, Artikelversion: 28. Mai 2025
Gesehen am 18.09.2025
Physical Description:Online Resource
ISSN:1095-8584
DOI:10.1016/j.yjmcc.2025.05.008

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