ArticleCells2020
Cell-Free Circulating Mitochondrial DNA: A Potential Blood-Based Marker for Atrial Fibrillation.
Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 62 citations in OpenAlex.
- Psychological stress induced mitochondrial response in humans and its medial prefrontal biomarker correlates.Translational psychiatry · 2026Article
- Review
- Sigma1R restores mitochondrial energy metabolism via the IRE1α/XBP1 pathway.Scientific reports · 2025Article
- Metabolic Remodeling and Mitochondrial Stress in Atrial Fibrillation: Mechanisms and Translational Targets.Reviews in cardiovascular medicine · 2025Review
- Circulating mitochondrial cell-free DNA levels are associated with the recurrence of atrial fibrillation after catheter ablation for atrial fibrillation.American heart journal plus : cardiology research and practice · 2025Article
- Mitochondrial DNA Dysfunction in Cardiovascular Diseases: A Novel Therapeutic Target.Antioxidants (Basel, Switzerland) · 2025Review
- Circulating cell-free mitochondrial DNA in diabetes mellitus: Current insights and unexplored frontiers.Journal of diabetes investigation · 2025Review
- Gestational chronic intermittent hypoxia triggers maternal inflammation and disrupts placental stress responses.American journal of physiology. Cell physiology · 2025Article
- The Interplay Between Pulmonary Hypertension and Atrial Fibrillation: A Comprehensive Overview.Cells · 2025Review
- Cell-free mitochondrial DNA may predict the risk of post-operative complications and outcomes in surgical aortic valve replacement patients.Scientific reports · 2025Article
- Mitochondrial damage mediates STING activation driving obesity-mediated atrial fibrillation.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2025Article
- Metabolic remodelling in atrial fibrillation: manifestations, mechanisms and clinical implications.Nature reviews. Cardiology · 2024Review
- Oxidative stress induces release of mitochondrial DNA into the extracellular space in human placental villous trophoblast BeWo cells.American journal of physiology. Cell physiology · 2024Article
- Modeling drug-induced mitochondrial toxicity with human primary cardiomyocytes.Science China. Life sciences · 2024Article
- The HF-AF ENERGY Trial: Nicotinamide Riboside for the Treatment of Atrial Fibrillation in Heart Failure Patients.Cardiovascular drugs and therapy · 2023Article
- Clinicopathological and circulating cell-free DNA profile in myositis associated with anti-mitochondrial antibody.Annals of clinical and translational neurology · 2023Article
- Activation of cell-free mtDNA-TLR9 signaling mediates chronic stress-induced social behavior deficits.Molecular psychiatry · 2023Article
- The genetic and phenotypic correlates of mtDNA copy number in a multi-ancestry cohort.HGG advances · 2023Article
- Intracellular to Interorgan Mitochondrial Communication in Striated Muscle in Health and Disease.Endocrine reviews · 2023Review
- Maternal and fetal mitochondrial gene dysregulation in hypertensive disorders of pregnancy.Physiological genomics · 2023Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atrial fibrillation (AF), the most common, progressive tachyarrhythmia is associated with serious complications, such as stroke and heart failure. Early recognition of AF, essential to prevent disease progression and therapy failure, is hampered by the lack of accurate diagnostic serum biomarkers to identify the AF stage. As we previously showed mitochondrial dysfunction to drive experimental and human AF, we evaluated whether cell-free circulating mitochondrial DNA (cfc-mtDNA) represents a potential serum marker. Therefore, the levels of two mtDNA genes, COX3 and ND1, were measured in 84 control patients (C), 59 patients undergoing cardiac surgery without a history of AF (SR), 100 paroxysmal (PAF), 116 persistent (PeAF), and 20 longstanding-persistent (LS-PeAF) AF patients undergoing either cardiac surgery or AF treatment (electrical cardioversion or pulmonary vein isolation). Cfc-mtDNA levels were significantly increased in PAF patients undergoing AF treatment, especially in males and patients with AF recurrence after AF treatment. In PeAF and LS-PeAF, cfc-mtDNA levels gradually decreased. Importantly, cfc-mtDNA in serum may originate from cardiomyocytes, as in vitro tachypaced cardiomyocytes release mtDNA in the medium. The findings suggest that cfc-mtDNA is associated with AF stage, especially in males, and with patients at risk for AF recurrence after treatment.
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