ArticleOxidative medicine and cellular longevity2022
Cardiac Fibroblasts Promote Ferroptosis in Atrial Fibrillation by Secreting Exo-miR-23a-3p Targeting SLC7A11.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 73 citations in OpenAlex.
- Extracellular Vesicles as Mediators of Pathophysiology and Disease Progression in Cardiovascular Diseases.International journal of molecular sciences · 2026Review
- Epigenetics in Atrial Fibrillation: Molecular Mechanisms and Therapeutic Avenues.Reviews in cardiovascular medicine · 2026Review
- Extracellular Vesicles in Myocardial Infarction: Dual Role in Ferroptosis Regulation and In Vivo Imaging.Diagnostics (Basel, Switzerland) · 2026Review
- Gut Microbiota-Non-Coding RNA Axis in Immune Modulation and Disease: From Mechanisms to Clinical Translation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Extracellular Vesicles as Biomarkers and Non-Surgical Therapeutics in Cardiovascular Diseases.Journal of clinical medicine · 2026Review
- MicroRNAs as novel therapeutic targets against inflammatory bowel disease through modulation of ferroptosis.Clinical and experimental medicine · 2026Review
- Pulmonary vein isolation with a pulsed field system leads to lower levels of miR-23a-3p in the left atrial blood compared to a cryoballoon.Scientific reports · 2026Article
- The Regulatory Landscape of Ferroptosis and Iron Homeostasis: Pathophysiological Mechanisms and Therapeutic Horizons in Cardiovascular Disease.Drug design, development and therapy · 2026Review
- Atrial Fibroblasts-Derived Extracellular Vesicles Exacerbate Atrial Arrhythmogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Mesenchymal stem cell-derived exosomes as a potential therapeutic strategy for ferroptosis.Stem cell research & therapy · 2025Review
- MicroRNAs at the crossroads of exercise and ferroptosis: a regulatory bridge.Clinical and experimental medicine · 2025Review
- Exosome-Based Therapy in Cardiovascular Diseases: A New Frontier in Cardiovascular Disease Treatment.Korean circulation journal · 2025Review
- An integrated bioinformatics approach for identification of key modulators and biomarkers involved in atrial fibrillation.Journal of cardiovascular and thoracic research · 2025Article
- The intersection of ferroptosis and non-coding RNAs: a novel approach to ovarian cancer.European journal of medical research · 2025Review
- SLC7A11 in Fibrosis: Molecular Mechanisms and Future Prospects.Aging and disease · 2025Review
- Roles and Therapeutic Targeting of Exosomes in Sepsis-Induced Cardiomyopathy.Journal of cellular and molecular medicine · 2025Review
- LncRNA Growth Arrest Specific 5 Promotes Glucose Metabolism Reprogramming Via the IGF2BP1/SIX1 Axis and Inhibits Ferroptosis of Endothelial Progenitor Cells Via the miR-23a-3p/SLC7A11 Axis in Coronary Heart Disease.Anatolian journal of cardiology · 2025Article
- Myocardial ferroptosis may exacerbate the progression of atrial fibrillation through isolevuglandins.European journal of medical research · 2025Review
- Epigenetic regulation and post-translational modifications of ferroptosis-related factors in cardiovascular diseases.Clinical epigenetics · 2025Review
- An emerging double‑edged sword role of ferroptosis in cardiovascular disease (Review).International journal of molecular medicine · 2025Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The exact mechanism of atrial fibrillation (AF) has been not well elucidated. Ferroptosis is an iron-dependent cell death due to excessive accumulation of peroxidized polyunsaturated fatty acids. However, the molecular mechanism underlying AF and ferroptosis has never been reported. Here, we established the rapid pacing model in vivo and vitro to investigate the relationship between AF and ferroptosis. In canine model of rapid atrial pacing, the content of malondialdehyde and total ions in the atrial tissue of the Pacing group was significantly increased and the exosome inhibitor GW4869 reduced ferroptosis, fibrosis, and inflammation and improved histological and electrophysiological remodeling. In rapid pacing h9c2 cells, the expression of antioxidative stress genes associated with ferroptosis presented sequential changes and proteins involved in ferroptosis such as FTH1, SLC7A11, and GPX4 were gradually depleted. Furthermore, pacing cardiac fibroblast-derived exosomes (CF-exos) exacerbated ferroptosis in h9c2 cells and pretreated pacing-CF-exos with GW4869 alleviated injury to h9c2 cells. In mechanism, our results demonstrated that pacing-CF-exos highly expressed miR-23a-3p by informatics analysis and experimental verification. Inhibitor-miR-23a-3p protected h9c2 cells from ferroptosis accompanying with upregulation of SLC7A11. In addition, SLC7A11 was shown to be the target gene of miR-23a-3p. In conclusion, our results suggest that CF-exos-miR-23a-3p may promote ferroptosis. The development of AF in a persistent direction could be prevented by intervening with exosomal miRNAs to reduce oxidative stress injury and ferroptosis.
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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.