ArticleFrontiers in immunology2022
MiR-93-5p promotes granulosa cell apoptosis and ferroptosis by the NF-kB signaling pathway in polycystic ovary syndrome.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 154 citations in OpenAlex.
- Orchestrating Ovarian Dysfunction- The Role of Programmed Cell Death in PCOS.Cell biochemistry and biophysics · 2026Article
- Mitochondria as integrative regulators of ferroptosis in the female reproductive system.Biology of reproduction · 2026Review
- Study on the Effects and Mechanisms of Sea Buckthorn Fruit Pulp in Improving Polycystic Ovary Syndrome.Food science & nutrition · 2026Article
- WTAP -mediated N6‑methylation of TRAF6 Facilitates Polycystic Ovary Syndrome by Inducing Ferroptosis.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- Sequencing and Differential Analysis of miRNA in the Ovaries of Kazakh Horses During Estrus and Anestrus States.Animals : an open access journal from MDPI · 2026Article
- Molecular Mechanisms Underlying Reproductive Dysfunction in Polycystic Ovary Syndrome.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Hyperhomocysteinemia reduces the high-quality embryo rate in PCOS patients undergoing IVF/ICSI: clinical evidence and a preliminary exploration of mechanisms in KGN cells.Journal of ovarian research · 2026Article
- Research Progress on Ferroptosis Regulation of Female Reproduction.Biological trace element research · 2026Review
- Natural Products in the Metabolic and Endocrine Modulation of Polycystic Ovary Syndrome: Current Perspectives.Nutrients · 2026Review
- Regulation of ferroptosis in colorectal cancer through therapeutic modulation and miRNA targeting.Biochemistry and biophysics reports · 2026Article
- Hyperandrogenemia Induces Trophoblast Ferroptosis and Early Pregnancy Loss in Patients With PCOS via CMA-Dependent FTH1 Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Ferroptosis in Myocardial Fibrosis: Mechanisms and Therapeutic Insights.Antioxidants (Basel, Switzerland) · 2026Review
- Exosomes for Polycystic Ovary Syndrome Treatment: Mechanisms and Therapeutic Potential.International journal of nanomedicine · 2026Review
- Article
- IL-33 Alleviates Sepsis-Induced Liver Injury by Regulating the NF-κB/BCL-2 Pathway.Current medicinal chemistry · 2026Article
- Mitochondria and polycystic ovary syndrome: The role of ferroptosis, inflammasomes, and endoplasmic reticulum stress.International journal of biological sciences · 2026Review
- The organelle oxidative-inflammatory network in polycystic ovary syndrome: from subcellular intercellular cascades to systemic comorbidities.Frontiers in immunology · 2026Review
- Upregulation of PLAU in granulosa cells disrupts steroid hormone synthesis and promotes apoptosis by activating NF-κB signaling pathway in PCOS.Journal of ovarian research · 2025Article
- Causal effects of ferroptosis-related traits on ovarian dysfunction: insights from integrating genome-wide Mendelian randomization, DNA methylation, gene expression, and proteome.Journal of ovarian research · 2025Article
- Rescuing fertility: C-Phycocyanin prevents ovarian damage through NRF2-mediated ferroptosis pathways in polycystic ovary syndrome models.Zoological research · 2025Article
20 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders in women of reproductive age. miR-93-5p has been reported to be elevated in granulosa cells of PCOS patients. However, the mechanism by which miR-93-5p drives granulosa cell (GC) progression remains unclear. Thus, this study focuses on the roles and mechanisms of miR-93-5p in the GCs of PCOS. Methods: KGN cells have similar ovarian physiological characteristics and are used to study the function and regulatory mechanism of GCs. In this study, KGN cells were transfected with si-NC, si-miR93-5p, oe-NC and oe-miR93-5p. A cell counting kit-8 assay, flow cytometry and western blotting were performed to observe the proliferation and apoptosis of KGN in different groups. Subsequently, the levels of reactive oxygen species, malondialdehyde, GPX4, SLC7A11 and Nrf2, which are indicators of ferroptosis, were measured by a dihydroethidium fluorescent dye probe, biochemical kit, western blotting and reverse transcription quantitative polymerase chain reaction. Ultimately, bioinformatic analysis and experimental methods were used to examine the interaction between miR-93-5p and the NF-κB signaling pathway. Results: miR-93-5p was upregulated in the GCs of PCOS patients. Overexpression of miR-93-5p promoted apoptosis and ferroptosis in KGN cells, while knockdown of miR-93-5p showed the reverse effect. Biological analysis and subsequent experiments demonstrated that miR-93-5p negatively regulates the NF- κB signaling pathway. Conclusion: miR-93-5p promotes the apoptosis and ferroptosis in GC by regulating the NF-κB signaling pathway. Silencing of miR-93-5p protects against GC dysfunction. Our study identified miR-93-5p as a new molecular target for improving the function of GCs in PCOS patients.
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