ArticlePeerJ2025
Downregulation of EB1 impedes Cx43 localization and cardiac conduction after hypothermic ischemia-reperfusion in rats.
Article in PeerJ, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Dnmt1 associatedEpigenetics · 2026Article
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8 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Background: Hypothermic ischemia-reperfusion arrhythmia is a common complication after cardiopulmonary bypass heart surgery, which can lead to hemodynamic disorders and even sudden cardiac death and is still not effectively prevented. This study aims to investigate the role and mechanisms of EB1 in hypothermic ischemia-reperfusion arrhythmia. Methods: 4-6 week old male Sprague-Dawley (SD) rats were randomly assigned to four groups with a control group receiving no treatment. In the treatment groups, the rats received an injection of a negative control adenovirus (AAV9-CON) or an adenoviral vector containing Mapre1 gene (AAV9-EB1) or an equal volume of saline Results: Following ischemia-reperfusion, EB1 expression was downregulated, accompanied by a reduction in Cx43. Overexpression of myocardial EB1 reduced the incidence of reperfusion arrhythmias and shortened their duration, which was associated with improved myocardial conduction. Male SD rats injected with AAV overexpressing EB1 had significantly higher levels of both total myocardial Cx43 and gap junction Cx43 after ischemia-reperfusion compared to the non-overexpression groups. Histological staining revealed lateralization of Cx43 in ischemia-reperfusion myocardium, which was corrected by EB1 overexpression. Additionally, EB1 overexpression increased the distribution of Cx43 at the IDs, overall reducing Cx43 remodeling. Moreover, EB1 overexpression can also alleviate microtubule damage caused by ischemia-reperfusion, which may be an important mechanism for the transport of Cx43 to the IDs. Conclusions: EB1 downregulation following hypothermic ischemia-reperfusion was accompanied by a reduction in gap junction Cx43. EB1 overexpression improved cardiac conduction and reduced reperfusion arrhythmias by promoting Cx43 localization to IDs, facilitating gap junctions (GJs) formation. These findings contribute to the development of new therapeutic targets for reperfusion arrhythmias.
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