ArticleMolecular therapy. Nucleic acids2021
Aberrant elevation of GDF8 impairs granulosa cell glucose metabolism via upregulating SERPINE1 expression in patients with PCOS.
Article in Molecular therapy. Nucleic acids, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
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- Pyruvate kinase M2 -mediated histone lactylation alters three-dimensional genomic architecture in polycystic ovary syndrome.Signal transduction and targeted therapy · 2025Article
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- Polycystic Ovarian Syndrome: A Review of Multi-omics Analyses.Reproductive sciences (Thousand Oaks, Calif.) · 2025Review
- Unraveling the complexity of follicular fluid: insights into its composition, function, and clinical implications.Journal of ovarian research · 2024Review
- Glial-Cell-Line-Derived Neurotrophic Factor Promotes Glioblastoma Cell Migration and Invasion via the SMAD2/3-SERPINE1-Signaling Axis.International journal of molecular sciences · 2024Article
- An integrated analysis of multiple datasets reveals novel gene signatures in human granulosa cells.Scientific data · 2024Article
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- Arsenic-Induced Thyroid Hormonal Alterations and Their Putative Influence on Ovarian Follicles in Balb/c Mice.Biological trace element research · 2024Article
- Essential Role of Granulosa Cell Glucose and Lipid Metabolism on Oocytes and the Potential Metabolic Imbalance in Polycystic Ovary Syndrome.International journal of molecular sciences · 2023Review
- Evaluation of the p53 pathway in polycystic ovarian syndrome pathogenesis and apoptosis enhancement in human granulosa cells through transcriptome data analysis.Scientific reports · 2023Article
- Multi-omics insights and therapeutic implications in polycystic ovary syndrome: a review.Functional & integrative genomics · 2023Review
- SERPINE1 and its co-expressed genes are associated with the progression of clear cell renal cell carcinoma.BMC urology · 2023Article
- Signaling pathways and targeted therapeutic strategies for polycystic ovary syndrome.Frontiers in endocrinology · 2023Review
- Editorial: Small molecules and peptides in paracrine/autocrine regulation of ovarian folliculogenesis.Frontiers in endocrinology · 2023Article
- A brief insight into the etiology, genetics, and immunology of polycystic ovarian syndrome (PCOS).Journal of assisted reproduction and genetics · 2022Review
- Disruption of O-GlcNAcylation Homeostasis Induced Ovarian Granulosa Cell Injury in Bovine.International journal of molecular sciences · 2022Article
- Myostatin: a multifunctional role in human female reproduction and fertility - a short review.Reproductive biology and endocrinology : RB&E · 2022Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clinical investigations have demonstrated that polycystic ovary syndrome (PCOS) is often accompanied by insulin resistance (IR) in more than 70% of women with PCOS. However, the etiology of PCOS with IR remains to be characterized. Growth differentiation factor 8 (GDF8) is an intraovarian factor that plays a vital role in the regulation of follicle development and ovulation. Previous studies have reported that GDF8 is a pathogenic factor in glucose metabolism disorder in IR patients. To date, the role of GDF8 on glucose metabolism of granulosa cell in PCOS patients remains to be determined. In the current study, we demonstrated that the expression and accumulation of GDF8 in human granulosa-lutein (hGL) cells and follicular fluid from PCOS patients were higher compared with those of non-PCOS women. GDF8 treatment caused glucose metabolism defects in hGL cells. Transcriptome sequencing results showed that SERPINE1 mediated GDF8-induced impairment of hGL glucose metabolism defects. Using pharmacological and small interfering RNA (siRNA)-mediated knockdown approaches, we demonstrated that GDF8 upregulated the expression of SERPINE1 via the ALK5-mediated SMAD2/3-SMAD4 signaling pathway. Interestingly, the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway was also activated with GDF8 treatment but did not participate in the effect of GDF8 on SERPINE1 expression. Our results also showed that TP53 was required for the GDF8-stimulated increase in SERPINE1 expression. Importantly, our study demonstrated that SB-431542 treatment significantly improved DHEA-induced PCOS-like ovaries. These findings support a potential role for GDF8 in metabolic disorders in PCOS.
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