ArticleInternational journal of molecular sciences2017
Oxidative Stress-Induced Afterdepolarizations and Protein Kinase C Signaling.
Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- A Computational Model of Oxidative Stress in a Human Ventricular Myocyte.bioRxiv : the preprint server for biology · 2026Article
- Article
- X-rays Stimulate Granular Secretions and Activate Protein Kinase C Signaling in Human Platelets.Current issues in molecular biology · 2023Article
- Nuclear factor erythroid 2-related factor 2-mediated signaling and metabolic associated fatty liver disease.World journal of gastroenterology · 2022Review
- The Nrf2 Pathway in Liver Diseases.Frontiers in cell and developmental biology · 2022Review
- Article
- Macrophages facilitate post myocardial infarction arrhythmias: roles of gap junction and KCa3.1.Theranostics · 2019Article
- The transient receptor potential melastatin 4 channel inhibitor 9-phenanthrol modulates cardiac sodium channel.British journal of pharmacology · 2018Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHydrogen peroxide (H₂O₂)-induced oxidative stress has been demonstrated to induce afterdepolarizations and triggered activities in isolated myocytes, but the underlying mechanisms remain not fully understood. We aimed to explore whether protein kinase C (PKC) activation plays an important role in oxidative stress-induced afterdepolarizations.
methodsAction potentials and ion currents of isolated rabbit cardiomyocytes were recorded using the patch clamp technique. H₂O₂ (1 mM) was perfused to induce oxidative stress and the specific classical PKC inhibitor, Gö 6983 (1 μM), was applied to test the involvement of PKC.
resultsH₂O₂ perfusion prolonged the action potential duration and induced afterdepolarizations. Pretreatment with Gö 6983 prevented the emergence of H₂O₂-induced afterdepolarizations. Additional application of Gö 6983 with H₂O₂ effectively suppressed H₂O₂-induced afterdepolarizations. H₂O₂ increased the late sodium current (I
conclusionsH₂O₂ induced afterdepolarizations via the activation of PKC and the enhancement of I
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