ArticleCell death & disease2023
Macrophages originated IL-33/ST2 inhibits ferroptosis in endometriosis via the ATF3/SLC7A11 axis.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 65 citations in OpenAlex.
- Research progress of ferroptosis in gynecological diseases.Annals of medicine · 2026Review
- PRDX4 ameliorates oxidative stress-induced injury in endometriosis: potential association with PTP1B oxidation and downstream phosphorylation cascades.Molecular and cellular biochemistry · 2026Article
- Deciphering the Role of ZEB1 as a Central Regulator of Epithelial-Mesenchymal Transition and Hormonal Resistance in Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- FIN56-induced ferroptosis suppresses the development of endometriosis by augmenting mitochondrial ROS and lipid peroxidation via the ACACA/ARID5A/NOX4 axis.Chinese medical journal · 2026Article
- MGST3 Promotes Endometriosis Progression by Suppressing Ferroptosis.Cell biochemistry and biophysics · 2026Article
- Recent insights in pathogenesis of endometriosis with focus on gut microbiota.Molecular biology reports · 2026Review
- Molecular Insights Into Endometriosis for Early Detection and Therapeutic Targets.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Andrographolide blocked the progression of endometriosis by promoting ferroptosis via inhibiting anabolism of serine.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Molecular mechanisms in endometriosis: linking JAK/STAT pathway, ferroptosis, and microbial dysbiosis.Molecular biology reports · 2026Review
- Dihydroartemisinin Alleviates Neuronal Damage and Seizures in Epileptic Mice by Inhibiting Ferroptosis via the SIRT1/FOXO1/SLC7A11/GPX4 Pathway.CNS neuroscience & therapeutics · 2026Article
- Elevated maternal pre-transfer serum lipid peroxidation is associated with implantation failure and early pregnancy loss.BMC medicine · 2026Article
- Research Advances in the Endometriotic Microenvironment: Synergistic Immune-Inflammatory-Angiogenic Interactions and their Therapeutic Translation.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Mechanistic insights into lipoprotein(a)-induced cardiomyocyte ferroptosis via ROS/p38/p53 signaling.Frontiers in medicine · 2026Article
- Estradiol Promotes Endometriosis ProgressionCurrent pharmaceutical biotechnology · 2026Article
- Mechanistic insights into ferroptosis and its therapeutic potential in hepatocellular carcinoma.Frontiers in immunology · 2026Review
- From gut-reproductive microbiota to ferroptosis: a comprehensive insight into the molecular-pathogenicity of endometriosis.Frontiers in immunology · 2026Review
- LRP1 as a potential diagnostic and immunomodulatory target in endometriosis: evidence from multi-omics and single-cell analyses.Frontiers in immunology · 2026Article
- Immune Suppression and Somatic Mutation in Endometriosis - An Opportunity for Personalized Immunotherapy.International journal of women's health · 2026Article
- The role of IL-33/ST2 signaling in female reproductive diseases.Frontiers in cell and developmental biology · 2026Review
- Regulated cell death in endometrial diseases: from molecular mechanisms to targeted therapies.Archives of toxicology · 2026Review
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometriosis is a gynecological inflammatory disease that is linked with immune cells, specifically macrophages. IL-33 secreted from macrophages is known to accelerate the progression of endometriosis. The periodic and repeated bleeding that occurs in women with endometriosis leads to excess iron in the microenvironment that is conducive to ferroptosis, a process related to intracellular ROS production, lipid peroxidation and mitochondrial damage. It is suggested that eESCs may specifically be able to inhibit ferroptosis. However, it is currently unclear whether IL-33 directly regulates ferroptosis to influence the disease course in endometriosis. In this study, eESCs co-cultured with macrophages or stimulated with IL-33/ST2 were observed to have increased cell viability and migration. Additionally, IL-33/ST2 decreased intracellular iron levels and lipid peroxidation in eESCs exposed to erastin treatment. Furthermore, IL-33/ST2 treatment resulted in a notable upregulation in SLC7A11 expression in eESCs due to the downregulation of negative transcription factor ATF3, thereby suppressing ferroptosis. The P38/JNK pathway activated by IL-33/ST2 was also found to inhibit the transcription factor ATF3. Therefore, we concluded that IL-33/ST2 inhibits the ATF3-mediated reduction in SLC7A11 transcript levels via the P38/JNK pathway. The findings reveal that macrophage-derived IL-33 upregulates SLC7A11 in eESCs through the p38/JNK/ATF3 pathway, ultimately resulting in protection against ferroptosis in eESCs. Moreover, we conducted an experiment using endometriosis model mice that showed that a combination of IL-33-Ab and erastin treatment alleviated the disease, showing the promise of combining immunotherapy and ferroptosis therapy.
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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.