ArticleOxidative medicine and cellular longevity2020
Thioridazine Induces Cardiotoxicity via Reactive Oxygen Species-Mediated hERG Channel Deficiency and L-Type Calcium Channel Activation.
Article in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 10 citations in OpenAlex.
- Atrial Fibrillation and Great Saphenous Vein Insufficiency: Exploration of Common Pathways in Hemodynamic Derangements and Systemic Inflammation.Reviews in cardiovascular medicine · 2026Review
- Synergistic Photothermal-Chemotherapy of Hepatocellular Carcinoma and Cancer Stem Cells via in situ pH-Responsive Hydrogels.International journal of nanomedicine · 2026Article
- Quercetin is a foe in the heart by targeting the hERG potassium channel.Iranian journal of basic medical sciences · 2024Article
- Preventing unfolded protein response-induced ion channel dysregulation to treat arrhythmias.Trends in molecular medicine · 2022Review
- Arginine Regulates NLRP3 Inflammasome Activation Through SIRT1 in Vascular Endothelial Cells.Inflammation · 2021Article
- QTc Interval Prolongation with Therapies Used to Treat Patients with Parkinson's Disease Psychosis: A Narrative Review.Neuropsychiatric disease and treatment · 2021Review
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Authors and funding
11 authors at 1 institution in 1 country.
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Abstract
Thioridazine (THIO) is a phenothiazine derivative that is mainly used for the treatment of psychotic disorders. However, cardiac arrhythmias especially QT interval prolongation associated with the application of this compound have received serious attention after its introduction into clinical practice, and the mechanisms underlying the cardiotoxicity induced by THIO have not been well defined. The present study was aimed at exploring the long-term effects of THIO on the hERG and L-type calcium channels, both of which are relevant to the development of QT prolongation. The hERG current (
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