ArticleFrontiers in physiology2013
Oxidative stress, fibrosis, and early afterdepolarization-mediated cardiac arrhythmias.
Article in Frontiers in physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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
19 citing papers in PubMed, 38 citations in OpenAlex.
- The role of cellular senescence in cardiovascular disease.Cell death discovery · 2025Review
- Detection, Isolation and Quantification of Myocardial Infarct with Four Different Histological Staining Techniques.Diagnostics (Basel, Switzerland) · 2024Article
- Detection, Isolation and Quantification of Myocardial Infarct with Four Different Histological Staining Techniques.bioRxiv : the preprint server for biology · 2024Article
- Mitochondrial Dysfunction in Heart Failure: From Pathophysiological Mechanisms to Therapeutic Opportunities.International journal of molecular sciences · 2024Review
- Arrhythmias among Older Adults Receiving Comprehensive Geriatric Care: Prevalence and Associated Factors.Clinics and practice · 2024Article
- In silico analysis of the contribution of cardiomyocyte-fibroblast electromechanical interaction to the arrhythmia.Frontiers in physiology · 2023Article
- Redox imbalance in patients with heart failure and ICD/CRT-D intervention. Can it be an underappreciated and overlooked arrhythmogenic factor? A first preliminary clinical study.Frontiers in physiology · 2023Article
- Multimodal imaging shows fibrosis architecture and action potential dispersion are predictors of arrhythmic risk in spontaneous hypertensive rats.The Journal of physiology · 2022Article
- Antioxidants in Arrhythmia Treatment-Still a Controversy? A Review of Selected Clinical and Laboratory Research.Antioxidants (Basel, Switzerland) · 2022Review
- Ageing Increases Cardiac Electrical Remodelling in Rats and Mice via NOX4/ROS/CaMKII-Mediated Calcium Signalling.Oxidative medicine and cellular longevity · 2022Article
- Suppression of ventricular arrhythmias by targeting late L-type Ca2+ current.The Journal of general physiology · 2021Article
- Handling of Ventricular Fibrillation in the Emergency Setting.Frontiers in pharmacology · 2019Review
- Arrhythmias in Patients ≥80 Years of Age: Pathophysiology, Management, and Outcomes.Journal of the American College of Cardiology · 2018Review
- Effect of myocyte-fibroblast coupling on the onset of pathological dynamics in a model of ventricular tissue.Scientific reports · 2017Article
- Evolution of strategies to improve preclinical cardiac safety testing.Nature reviews. Drug discovery · 2016Review
- Changes in Intracellular Na+ following Enhancement of Late Na+ Current in Virtual Human Ventricular Myocytes.PloS one · 2016Article
- Arrhythmogenesis in a catecholaminergic polymorphic ventricular tachycardia mutation that depresses ryanodine receptor function.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- A Comparative Study of Early Afterdepolarization-Mediated Fibrillation in Two Mathematical Models for Human Ventricular Cells.PloS one · 2015Article
- Ellagic acid improved arrhythmias induced by CaCL2 in the rat stress model.Avicenna journal of phytomedicineArticle
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Animal and clinical studies have demonstrated that oxidative stress, a common pathophysiological factor in cardiac disease, reduces repolarization reserve by enhancing the L-type calcium current, the late Na, and the Na-Ca exchanger, promoting early afterdepolarizations (EADs) that can initiate ventricular tachycardia and ventricular fibrillation (VT/VF) in structurally remodeled hearts. Increased ventricular fibrosis plays a key facilitatory role in allowing oxidative-stress induced EADs to manifest as triggered activity and VT/VF, since normal non-fibrotic hearts are resistant to arrhythmias when challenged with similar or higher levels of oxidative stress. The findings imply that antifibrotic therapy, in addition to therapies designed to suppress EAD formation at the cellular level, may be synergistic in reducing the risk of sudden cardiac death.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.