ArticleBioMed research international2022
Upregulated Fibulin-1 Increased Endometrial Stromal Cell Viability and Migration by Repressing EFEMP1-Dependent Ferroptosis in Endometriosis.
Article in BioMed research international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Research progress of ferroptosis in gynecological diseases.Annals of medicine · 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
- Fibulin-1 Improves Caerulein-Induced Acute Pancreatitis In Vitro by Inhibiting Ferroptosis.Journal of biochemical and molecular toxicology · 2026Article
- MGST3 Promotes Endometriosis Progression by Suppressing Ferroptosis.Cell biochemistry and biophysics · 2026Article
- Tiaojing Cuyun Recipe inhibits ferroptosis through SLC7A11/GSH/GPX4 axis to improve endometrial receptivity of mice with embryo implantation dysfunction.Journal of traditional and complementary medicine · 2026Article
- HAGLR promotes endometriosis progression via the miR-185-5p/VEGFA axis and serves as a potential diagnostic biomarker.BMC women's health · 2026Article
- Investigating the role of EGFR signalling in muscle dystrophies: implications for Duchenne muscular dystrophy.Cell death & disease · 2026Article
- The Role of Ferroptosis in Women's Health and Diseases.MedComm · 2025Review
- Impact of Static Myoblast Loading on Protein Secretion Linked to Tenocyte Migration.Journal of proteome research · 2025Article
- Erastin-induced multi-pathway cell death in endometriosis: a mechanistic and translational narrative review.Frontiers in medicine · 2025Review
- PDLIM3 knockdown promotes ferroptosis in endometriosis progression via inducing Gli1 degradation and blocking Hedgehog signaling pathway.Journal of assisted reproduction and genetics · 2024Article
- FBLN1 regulates ferroptosis in acute respiratory distress syndrome by reducing free ferrous iron by inhibiting the TGF-β/Smad pathway.PloS one · 2024Article
- Macrophages originated IL-33/ST2 inhibits ferroptosis in endometriosis via the ATF3/SLC7A11 axis.Cell death & disease · 2023Article
- Current Understanding of and Future Directions for Endometriosis-Related Infertility Research with a Focus on Ferroptosis.Diagnostics (Basel, Switzerland) · 2023Review
- Crosstalk between ferroptosis and steroid hormone signaling in gynecologic cancers.Frontiers in molecular biosciences · 2023Review
- The role of iron in the pathogenesis of endometriosis: a systematic review.Human reproduction open · 2023Article
- Iron-overloaded follicular fluid increases the risk of endometriosis-related infertility by triggering granulosa cell ferroptosis and oocyte dysmaturity.Cell death & disease · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometriosis (EMS) is a prevalent disease in women characterized by the presence of endometrial stroma and glands outside the uterus. Recent studies have showed that EMS is correlated with the resistance of endometrial stromal cells (ESCs) to ferroptosis, an iron-dependent nonapoptotic cell death. Fibulin-1 (FBLN1) is a newly identified target regulated by progesterone in the process of ESC decidualization. However, the role of FBLN1 in regulating ESC ferroptosis and EMS remains unclear. In the present study, the gene expression profiles of GSE58178, GSE23339, and GSE25628 were downloaded from the Gene Expression Omnibus (GEO) database, and the commonly differential genes were identified using Venn diagram analysis. The role of FBLN1 in ESC viability and migration was evaluated using Cell Counting Kit-8, transwell, and western blot analysis. We found that the FBLN1 expression was increased significantly in eutopic and ectopic endometrial tissues of patients with EMS compared with normal endometrium. FBLN1 overexpression in normal ESCs (NESCs) promoted cell viability and migration, whereas FBLN1 inhibition in ectopic ESCs (EESCs) decreased cell viability and migration. Furthermore, FBLN1 inhibition facilitated EESC death by triggering ferroptosis, as evidenced by increased Fe
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