ArticleCell death & disease2022
TFRC upregulation promotes ferroptosis in CVB3 infection via nucleus recruitment of Sp1.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.
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Who cites it
77 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.
- Genome-Scale Meta-analysis of Host Responses to Staphylococcus aureus Identifies Pathways for Host-Directed Therapeutic Targeting.The Journal of infectious diseases · 2025Pooled it
- The TRPM2-PARP-1 Axis Involvement in Bisphenol A and Nonylphenol-Induced Ferroptosis in Trigeminal Ganglion Cells.Journal of applied toxicology : JAT · 2026Article
- PEDV envelope protein promotes viral replication by remodeling host iron homeostasis via the TRIM28-KLF15-FPN axis.Journal of virology · 2026Article
- Induction of transferrin receptor 1-mediated ferroptosis by ultrasound-triggered microbubble destruction sensitizes glioblastoma to radiotherapy.Molecular biomedicine · 2026Article
- Review
- Rapid evolution of lncRNAs introduces novel regulatory inputs into ancestral cancer pathways.Science advances · 2026Article
- Rotavirus infection induces ferroptosis through NCOA4-mediated ferritinophagy in IPEC-J2 cells.Journal of animal science and biotechnology · 2026Article
- Curcumin Protects Mouse Spermatogonia from Triptolide-Induced Injury Through Modulation of Ferroptosis-Related Pathways.Biology · 2026Article
- TRMT10C promotes mitochondrial fission through transferrin receptor m1A methylation modification and aggravates the progression of atrial fibrillation.Journal of cell communication and signaling · 2026Article
- Article
- Ascites protects against ferroptosis and enables the peritoneal growth of ovarian cancer.Nature communications · 2026Article
- Article
- The Role of Ferroptosis in Diabetes Pathogenesis: Therapeutic Implications of Hydrogen Sulfide and Its Reactive Metabolites.Antioxidants (Basel, Switzerland) · 2026Review
- Pesticides Drive Liver Diseases Through Non-Apoptotic Regulated Cell Death Pathways.Diseases (Basel, Switzerland) · 2026Review
- Gastrodin improves learning and memory in sleep-deprived mice through suppression of ferroptosis in hippocampal neurons via Nrf2.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Recent progress in understanding ferroptosis mechanisms in infectious diseases.Frontiers in cellular and infection microbiology · 2026Review
- The role of glucose metabolic reprogramming in myocarditis and advances in therapeutic strategies.Frontiers in cardiovascular medicine · 2026Review
- Identification of TIMP1 as a Key Regulator of Ferroptosis in Ulcerative Colitis Through Bioinformatics and Functional Experiments.Gastroenterology research and practice · 2026Article
- Evaluation of Polystyrene Nanoplastics Induced Cardiotoxicity Under Different Dietary Patterns in Mice.Toxics · 2025Article
- Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CVB3 is a single positive-strand enterovirus, and a common pathogen in myocarditis etiology. Although a number of antiviral candidates are under development, specific targeted therapy is not available for CVB3. Ferroptosis is a new type of regulatory cell death discovered in recent years. In this study, our team provided the first evidence that ferroptosis existed in CVB3 infection in vivo and in vitro by iron overload, and massive accumulation of lipid peroxides. Mechanistically, we construct a classical model of HeLa cells following a time-course infection (6, 12, 24, 36, 48 h) with CVB3 (MOI = 10). We demonstrated that the TFRC gene plays an important role in promoting ferroptosis in CVB3 infection and downregulation of TFRC attenuated the ferroptosis. Interestingly, we observed that TFRC was nuclear translocation induced by the CVB3, which was predominantly localized in the cell membrane, but redistributed to the nucleus during CVB3 infection. Moreover, we found that the transcription factor Sp1 was an essential factor that could bind to the TFRC promoter and upregulate the TFRC transcription. Collectively, these results suggest that the Sp1/TFRC/Fe axis may provide a new target for the development of therapies against CVB3 infection.
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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.