ArticleInternational journal of molecular sciences2023
Developing Pharmacological Therapies for Atrial Fibrillation Targeting Mitochondrial Dysfunction and Oxidative Stress: A Scoping Review.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 13 citations in OpenAlex.
- Exploring the role of CaMKII in exercise-induced cardioprotection.Human cell · 2026Review
- Humanin and MOTS-c Attenuate Atrial Fibrillation by Suppressing Fibrosis and Mitochondrial Dysfunction.Biomedicines · 2026Article
- Elucidating Trigonelline's Therapeutic Mechanisms for Traumatic Brain Injury Through Integrated Network Pharmacology and In Vivo Validation.CNS neuroscience & therapeutics · 2026Article
- Saroglitazar Mitigated Cyclophosphamide-Induced Testicular Injury: Crosstalk Between Oxidative Stress, Inflammation and Apoptosis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Targeting the Ubiquitin-Proteasome System in Atrial Fibrillation: Mechanistic Insights and Translational Perspectives.Current issues in molecular biology · 2025Review
- Arrhythmia-Induced Cardiomyopathy in Atrial Fibrillation: Pathogenesis, Diagnosis, and Treatment.Life (Basel, Switzerland) · 2025Review
- Alginate-based hydrogels loaded with human β-defensin-2 promote healing of MRSA-infected wounds in a diabetic model: a preclinical proof-of-concept study.Clinical and experimental medicine · 2025Article
- Metabolic-dysfunction associated steatotic liver disease and atrial fibrillation: A review of pathogenesis.World journal of cardiology · 2025Review
- CYBB identified as a key immune hub gene linking lung cancer and atrial fibrillation.Journal of cardiothoracic surgery · 2025Article
- Administration withCytotechnology · 2025Article
- Mitochondrial Dysfunction in Atrial Fibrillation: The Need for a Strong Pharmacological Approach.Biomedicines · 2024Review
- Review
- Review
- Causal gene identification using mitochondria-associated genome-wide mendelian randomization in atrial fibrillation.Frontiers in pharmacology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atrial fibrillation (AF) is a cardiac arrhythmia caused by electrophysiological anomalies in the atrial tissue, tissue degradation, structural abnormalities, and comorbidities. A direct relationship exists between AF and altered mitochondrial activity resulting from membrane potential loss, contractile dysfunction, or decreased ATP levels. This review aimed to elucidate the role of mitochondrial oxidative mechanisms in AF pathophysiology, the impact of mitochondrial oxidative stress on AF initiation and perpetuation, and current therapies. This review followed the Preferred Reporting Items for Systematic Reviews and the Meta-Analysis Extension for Scoping Reviews. PubMed, Excerpta Medica Database, and Scopus were explored until June 2023 using "MESH terms". Bibliographic references to relevant papers were also included. Oxidative stress is an imbalance that causes cellular damage from excessive oxidation, resulting in conditions such as AF. An imbalance in reactive oxygen species production and elimination can cause mitochondrial damage, cellular apoptosis, and cardiovascular diseases. Oxidative stress and inflammation are intrinsically linked, and inflammatory pathways are highly correlated with the occurrence of AF. AF is an intricate cardiac condition that requires innovative therapeutic approaches. The involvement of mitochondrial oxidative stress in the pathophysiology of AF introduces novel strategies for clinical treatment.
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Registered trials
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