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: | , , , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
July 2025
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| 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 |
MARC
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| 245 | 1 | 4 | |a The role of connexin-43 in modeling arrhythmogenic diseases with induced pluripotent stem cell-derived cardiomyocytes |c Xijian Ke, Jonathan S. Baillie, Enrico D. Lemma, Martin Bastmeyer, Markus Hecker, Nina D. Ullrich |
| 246 | 3 | 3 | |a The role of connexin-fortythree in modeling arrhythmogenic diseases with induced pluripotent stem cell-derived cardiomyocytes |
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| 520 | |a 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. | ||
| 650 | 4 | |a Arrhythmogenic disease | |
| 650 | 4 | |a Cx43 | |
| 650 | 4 | |a Gap junctions | |
| 650 | 4 | |a iPSC-cardiomyocytes | |
| 650 | 4 | |a microRNA-1 | |
| 650 | 4 | |a Na1.5 | |
| 650 | 4 | |a Patch clamp | |
| 700 | 1 | |a Baillie, Jonathan S. |e VerfasserIn |4 aut | |
| 700 | 1 | |a Lemma, Enrico D. |e VerfasserIn |4 aut | |
| 700 | 1 | |a Bastmeyer, Martin |e VerfasserIn |4 aut | |
| 700 | 1 | |a Hecker, Markus |d 1960- |e VerfasserIn |0 (DE-588)1071693344 |0 (DE-627)826266037 |0 (DE-576)433260319 |4 aut | |
| 700 | 1 | |a Ullrich, Nina D. |e VerfasserIn |0 (DE-588)1130195619 |0 (DE-627)884562549 |0 (DE-576)486667251 |4 aut | |
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