ArticleExperimental animals2025
Transferrin receptor knockdown attenuates atrial fibrillation by inhibiting cardiomyocyte ferroptosis and atrial fibrosis.
Article in Experimental animals, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Ferroptosis in Myocardial Fibrosis: Mechanisms and Therapeutic Insights.Antioxidants (Basel, Switzerland) · 2026Review
- Organelle-specific regulation of ferroptosis.Biology direct · 2026Review
- Beyond Iron: The Roles of CD71 in the Pathophysiology of Cancer-A Comprehensive Review.Journal of clinical medicine · 2025Review
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Authors and funding
6 authors.
Funding
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Abstract
Atrial fibrillation (AF) is a common arrhythmia in clinical. Its most important pathophysiological factor is atrial fibrosis. Transferrin receptor (TFRC) promotes ferroptosis by facilitating iron uptake. Its role in AF is unknown. TFRC expression in Angiotensin II (Ang II)-induced AF mice was significantly upregulated. TFRC knockdown significantly reduced AF occurrence. TFRC silence ameliorated myocardial fibrosis by inhibiting transforming growth factor-β1 (TGF-β1)/Smad2 pathway in vivo. TFRC interference reduced ferroptosis by inhibiting lipid oxidation product generation in vivo. Ang II-induced HL-1 cardiomyocyte model was employed to simulate an in vivo situation. The in vitro results were consistent with the in vivo results. Forkhead box O3 (FOXO3) was reported to protect atrium against fibrosis and participate in ferroptosis. FOXO3 exerted transcriptional repressive activity by binding to TFRC promoter. FOXO3 overexpression protected HL-1 cells against ferroptosis, which was reversed by TFRC overexpression. In summary, TFRC knockdown reduces AF occurrence by ameliorating atrial fibrosis through inhibiting cardiomyocyte ferroptosis under FOXO3 regulation.
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