ArticleJournal of ovarian research2025
BFGF mitigates CTX-induced ovarian cytotoxicity via SERPINE1/HIF-1 and Nrf-2/HO-1 signaling pathways.
Article in Journal of ovarian research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Targeted delivery of RGD-JEG-3-EVs for placental vascular regeneration in preeclampsia: from molecular mechanism toward therapy.Apoptosis : an international journal on programmed cell death · 2026Article
- DNA Methylation, SERPING1 Expression, and Immune-related Traits in Osteoporosis: A Mendelian Randomization Study And SupportiveEndocrine, metabolic & immune disorders drug targets · 2026Article
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Authors and funding
5 authors.
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Abstract
Chemotherapy-induced ovarian damage is a significant concern for female cancer patients, often resulting in infertility, hormonal imbalance, and premature ovarian failure. Cyclophosphamide (CTX), a widely used chemotherapeutic agent, is highly effective against tumors but causes severe ovarian cytotoxicity. This study explores the protective effects of basic fibroblast growth factor (BFGF) and its underlying mechanisms in mitigating CTX-induced ovarian damage. BFGF treatment significantly enhanced cell viability, reduced apoptosis, and restored mitochondrial membrane potential in CTX-treated ovarian cells. Transcriptomic analysis revealed that BFGF activated the SERPINE1/HIF-1 signaling pathway, promoting angiogenesis, reducing apoptotic signaling, and enhancing cell cycle progression by upregulating Cyclin D1 and CDK4. Additionally, BFGF activated the Nrf-2/HO-1 pathway, boosting cellular defenses against oxidative stress and mitigating mitochondrial dysfunction. Functional studies confirmed that the inhibition of SERPINE1 or BFGF abrogated these protective effects, underscoring the critical roles of these pathways. These findings demonstrate that BFGF protects ovarian cells from CTX-induced damage by modulating the Serpin Family E Member 1 (SERPINE1)/Hypoxia-inducible factor 1 (HIF-1) and Nuclear factor erythroid 2-related factor 2 (Nrf-2)/Heme Oxygenase 1 (HO-1) pathways, reducing apoptosis, and enhancing cell survival, providing a promising foundation for developing BFGF-based therapies to preserve ovarian function and fertility in female cancer patients undergoing chemotherapy.
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Registered trials
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