ArticleFrontiers in pharmacology2025
Abnormal Ca
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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Authors and funding
12 authors.
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Abstract
Background: Citalopram (CIT) is widely used as an anti-depressant and has been reported to be associated with QT interval prolongation and increased vulnerability of torsades de pointes (TdP), although the underlying mechanism remains unclear. Objective: The aim of this study is to determine the proarrhythmic properties and underlying mechanisms of CIT. Methods: Mice were intraperitoneally injected with CIT or saline (SAL) for 4 weeks. Echocardiograms and electrocardiograms were performed to evaluate the cardiac electrophysiological and hemodynamic properties. Proarrhythmic mechanisms of CIT were then explored using optical mapping. Finally, transcriptomic array, RT-qPCR, and whole-cell patch-clamp were conducted to explore and validate the potential ionic mechanisms of CIT-related electrical abnormalities. Results: CIT treatment induced QT prolongation and increased the vulnerability of cardiac arrhythmias in the absence of structural or hemodynamic changes. Optical mapping showed that action potential duration (APD) and Ca Conclusion: CIT treatment resulted in QT prolongation and higher susceptibility of ventricular arrhythmia. Regions with serious cardiac alternans were mainly responsible for initiation of CIT-related arrhythmias. Abnormal Ca
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