ArticleCell death and differentiation2023
N6-Methyladenosine-modified circSAV1 triggers ferroptosis in COPD through recruiting YTHDF1 to facilitate the translation of IREB2.
Article in Cell death and differentiation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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Who cites it
85 citing papers in PubMed, 136 citations in OpenAlex.
- Cuproptosis and ferroptosis: signal pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
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- Exploring Ferroptosis: A Key Mechanism in Respiratory System Diseases and its Therapeutic Potential.Applied biochemistry and biotechnology · 2026Review
- AARS1-Mediated RUNX3 K193 Lactylation Enhances the Activation and Cytotoxicity of CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Circulating circRNAs at the frontier of cancer detection, prognosis, and therapy.Chinese medical journal · 2026Review
- BMSC-derived exosomal METTL3 synergizes with Sevoflurane to inhibit ferroptosis in pulmonary ischemia/reperfusion injury by enhancing USP7 N6-methyladenosine modification.Apoptosis : an international journal on programmed cell death · 2026Article
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- HHIP's dynamic role in epithelial wound healing reveals a potential mechanism of COPD susceptibility.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
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- CircAFF4 inhibits lung cancer progression via destabilizing GPX4 and triggering ferroptosis.Biology direct · 2026Article
- Morinda officinalis polysaccharide improves osteoporosis by enhancing m⁶A-modified SOCS5 mRNA stability via regulating the hsa_circ_0001165/IGF2BP2 axis.Molecular genetics and genomics : MGG · 2026Article
- m⁶A-Modified hsa_circ_0002694 facilitates OSCC progression via the METTL14/YTHDC1/miR-616-3p/c-Myc axis.Head & face medicine · 2026Article
- Circular RNAs in metabolic health: bridging the gap between molecular biology and therapy.Cell death & disease · 2026Review
- Bronchial epithelial-derived exosomal SLC6A14 promotes airway inflammation and mucus hypersecretion via the ZFP36L1/IL-8 axis.Functional & integrative genomics · 2026Article
- From locus to gene: causal inference and experimental validation prioritize PSMA4 as a candidate target in lung adenocarcinoma.American journal of cancer research · 2026Article
- Emerging functions of m6A-modified circRNAs and their targeting strategies in lung cancer.Frontiers in cell and developmental biology · 2026Review
- A Cross-Tissue Transcriptome Association Study Revealed Novel Susceptibility Genes for Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2026Article
- Functional roles and mechanisms of circRNA-protein interactions in cancer progression and tumor immune regulation.Frontiers in immunology · 2026Review
- Ferroptosis in diabetic retinopathy: from pathogenic mechanisms to translational prospects.Frontiers in endocrinology · 2026Review
25 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial cell damage-initiated chronic obstructive pulmonary disease (COPD) is implicated in regulated cell death (RCD) including ferroptosis triggered by complex gene-environment interactions. Our data showed that iron overload and ferroptosis are associated with COPD progression in COPD patients and in experimental COPD. Furthermore, we found that, in lung tissues of COPD patients, circSAV1 was associated with COPD progression by circRNA-seq screening. Knockdown of circSAV1 reversed cigarette smoke extract (CSE)-induced ferroptosis. Mechanistically, m6A-modified circSAV1 formed an RNA-protein ternary complex of circSAV1/YTHDF1/IREB2 to facilitate the translation of IREB2 mRNA. Elevated protein levels of IREB2 disrupted iron homeostasis, resulting in accumulation of a labile iron pool (LIP) and lipid peroxidation, which contribute to ferroptosis. Here we demonstrate, by use of an experimental COPD model induced by cigarette smoke (CS), that silencing of circSAV1 and the treatment with deferoxamine (DFO) blocked CS-induced ferroptosis of lung epithelial cells, which attenuated COPD progression in mice. Our results reveal that N6-methyladenosine-modified circSAV1 triggers ferroptosis in COPD through recruiting YTHDF1 to facilitate the translation of IREB2, indicating that circSAV1 is a mediator of ferroptosis and that circSAV1-dependent ferroptosis is a therapeutic target for COPD. In lung epithelial cell, m6A-modified circSAV1, via recruiting YTHDF1, induces the formation of a circSAV1/YTHDF1/IREB2 mRNA protein ternary complex, which promotes translation of IREB2 mRNA. Further, elevated IREB2 contributes to the accumulation of a labile iron pool (LIP) and lipid peroxidation, then triggers ferroptosis of lung epithelial cells. The ferroptosis of airway epithelial cells and alveolar epithelial cells induces airway remodeling and emphysema, respectively, which causes COPD.
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