ReviewBiomedicines2024
Mitochondrial Dysfunction in Atrial Fibrillation: The Need for a Strong Pharmacological Approach.
Review in Biomedicines, 2024. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed.
- ALYREF stabilizes MZF1 via m5C modification to exacerbate cardiac remodeling and atrial fibrillation in heart failure.Cellular and molecular life sciences : CMLS · 2026Article
- Pharmacogenomics of Atherosclerotic Plaque: Pathophysiological Background and Therapeutic Perspectives.Current atherosclerosis reports · 2026Review
- Inflammation, Endothelial Dysfunction, and Platelet Dysregulation in Atrial Fibrillation with Chronic Kidney Disease: Toward a Biology-Informed Anticoagulation Strategy.Life (Basel, Switzerland) · 2026Review
- Clinical Impact of Semaglutide Beyond Glycemic Control: A Critical Analysis of Oncogenic Potential and Mitigation of Cardiotoxicity.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Precision Monitoring Strategies for Chemotherapy-Induced Cardiotoxicity: A Review of Molecular Indicators for Early Detection and Risk Stratification.Reviews in cardiovascular medicine · 2026Review
- Metabolic Remodeling and Mitochondrial Stress in Atrial Fibrillation: Mechanisms and Translational Targets.Reviews in cardiovascular medicine · 2025Review
- Mitochondria-Targeted Antioxidants Prevent Tachypacing-Induced Contractile Dysfunction in In Vitro Cardiomyocyte and In VivoAntioxidants (Basel, Switzerland) · 2025Article
- Atrial Fibrillation in COVID-19: Mechanisms, Clinical Impact, and Monitoring Strategies.Biomedicines · 2025Review
- Central Role of Mitochondrial Oxidative Stress in the Pathophysiology of Disorders.Biomedicines · 2025Article
- Atrial Septal Defect and Heart Rhythm Disorders: Physiopathological Linkage and Clinical Perspectives.Biomedicines · 2025Review
- Factor XI and Cancer: Physiopathological Linkage and Clinical Perspectives.Journal of clinical medicine · 2025Review
- Atrial Fibrillation and Cancer: Pathophysiological Mechanism and Clinical Implications.Journal of clinical medicine · 2025Review
- Atrial Fibrillation in Diabetes: Pathogenesis and Targeted Rhythm Control Strategies.Current issues in molecular biology · 2025Review
- Heart Failure and Wide QRS: Clinical and Pharmacological Perspectives.Biomedicines · 2025Review
- Takotsubo Syndrome and Oxidative Stress: Physiopathological Linkage and Future Perspectives.Antioxidants (Basel, Switzerland) · 2025Review
- Evaluating inflammatory status to predict atrial fibrillation recurrence following ablation: The role of systemic immune-inflammation index.World journal of cardiology · 2025Article
- Serum Lipids, Inflammation, and the Risk of Atrial Fibrillation: Pathophysiological Links and Clinical Evidence.Journal of clinical medicine · 2025Review
- Ion channels and atrial fibrillation: mitophagy as a key mediator.Frontiers in physiology · 2025Article
- Relationship Between Left Atrial Strain and Atrial Fibrillation: The Role of Stress Echocardiography.Diagnostics (Basel, Switzerland) · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite great progress in treating atrial fibrillation (AF), especially with the development of increasingly effective invasive techniques for AF ablation, many unanswered questions remain regarding the pathogenic mechanism of the arrhythmia and its prevention methods. The development of AF is based on anatomical and functional alterations in the cardiomyocyte resulting from altered ionic fluxes and cardiomyocyte electrophysiology. Electric instability and electrical remodeling underlying the arrhythmia may result from oxidative stress, also caused by possible mitochondrial dysfunction. The role of mitochondrial dysfunction in the pathogenesis of AF is not yet fully elucidated; however, the reduction in AF burden after therapeutic interventions that improve mitochondrial fitness tends to support this concept. This selected review aims to summarize the mechanisms of mitochondrial dysfunction related to AF and the current pharmacological treatment options that target mitochondria to prevent or improve the outcome of AF.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.