ArticleProceedings of the National Academy of Sciences of the United States of America2022
Mitochondrial outer membrane protein FUNDC2 promotes ferroptosis and contributes to doxorubicin-induced cardiomyopathy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. 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, 140 citations in OpenAlex.
- Cuproptosis and ferroptosis: signal pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Ferroptosis: Newly Emerged Regulator for Human Disease.MedComm · 2026Review
- Cardiovascular Toxicity in Cancer Therapy: Potential Mechanisms of Ferroptosis and Treatment Strategies.Cells · 2026Review
- The Interplay of Programmed Cell Death Networks in Cardiovascular Diseases: Mechanisms and Therapeutic Opportunities.Reviews in cardiovascular medicine · 2026Review
- 1,8-Cineole Alleviates PA-Induced Lipid Accumulation, Oxidative Stress, and Inflammation via the TLR4/MyD88/NF-κB Signaling Pathway.Molecules (Basel, Switzerland) · 2026Article
- Research Progress on the Role of Traditional Chinese Medicine in Regulating Ferroptosis in Cardiovascular Diseases.Biology · 2026Review
- EDTA-Functionalized Nanoscale Metal-Organic Framework for Onco-Cardiology via Radiochemotherapy Synergy and Spatiotemporally Matched Iron Chelation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Phenothiazine alleviates cisplatin-mediated acute kidney injury by inhibiting ferroptosis.Cell and tissue research · 2026Article
- SLC25A11-mediated reprogramming of mitochondrial redox state and lipid peroxidation confers NRF2-dependent ferroptosis resistance in biliary tract cancer.Cellular & molecular biology letters · 2026Article
- METTL3-m6A-SLC25A11 Axis Promotes Chronic Hypoxia-Induced Cardiomyocyte Ferroptosis.Journal of the American Heart Association · 2026Article
- Bridging innate immunity and iron-dependent death: the interplay between cyclic GMP-AMP synthase-stimulator of interferon genes nexus and ferroptosis in cancer and inflammation.Frontiers in cell and developmental biology · 2026Review
- The interplay mechanisms between gut microbiota and ferroptosis in inflammatory bowel disease.Frontiers in immunology · 2026Review
- Mitochondrial dysfunction-driven PANoptosis in doxorubicin-induced cardiotoxicity: mechanistic insights and intervention strategies.Frontiers in pharmacology · 2026Review
- Mitochondrial outer membrane protein FUNDC2 contributes to ferroptosis as a potential upstream regulator in retinitis pigmentosa.International journal of ophthalmology · 2026Article
- Ferroptosis in Cardiovascular Diseases and Ferroptosis-Related Intervention Approaches.Cardiovascular drugs and therapy · 2025Review
- Article
- Ferroptosis: biology and role in liver disease.Journal of gastroenterology · 2025Review
- Superoxide Activates Ferroptosis via the Haber-Weiss Reaction and Enhances Age-Related Macular Degeneration.Aging cell · 2025Article
- Review
- EBBP-Mediated Integrated Stress Response Attenuates Anthracycline-Induced Cardiotoxicity by Inhibiting the Ferroptosis of Cardiomyocytes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
25 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ferroptosis is an iron-dependent programmed necrosis characterized by glutathione (GSH) depletion and lipid peroxidation (LPO). Armed with both the pro- and antiferroptosis machineries, mitochondria play a central role in ferroptosis. However, how mitochondria sense the stress to activate ferroptosis under (patho-)physiological settings remains incompletely understood. Here, we show that FUN14 domain-containing 2, also known as HCBP6 (FUNDC2), a highly conserved and ubiquitously expressed mitochondrial outer membrane protein, regulates ferroptosis and contributes to doxorubicin (DOX)-induced cardiomyopathy. We showed that knockout of FUNDC2 protected mice from DOX-induced cardiac injury by preventing ferroptosis. Mechanistic studies reveal that FUNDC2 interacts with SLC25A11, the mitochondrial glutathione transporter, to regulate mitoGSH levels. Specifically, knockdown of SLC25A11 in FUNDC2-knockout (KO) cells reduced mitoGSH and augmented erasin-induced ferroptosis. FUNDC2 also affected the stability of both SLC25A11 and glutathione peroxidase 4 (GPX4), key regulators for ferroptosis. Our results demonstrate that FUNDC2 modulates ferroptotic stress via regulating mitoGSH and further support a therapeutic strategy of cardioprotection by preventing mitoGSH depletion and ferroptosis.
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