ArticleCell proliferation2025
GPD1L-Mediated Glycerophospholipid Metabolism Dysfunction in Women With Diminished Ovarian Reserve: Insights From Pseudotargeted Metabolomic Analysis of Follicular Fluid.
Article in Cell proliferation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Molecular characteristics of follicular fluid in advanced maternal age women with different ovarian reserves: a multi-omics study.BMC women's health · 2026Article
- Multi-omics atlas of ovarian cellular and molecular responses to diabetes.Molecular metabolism · 2026Article
- ROS: their roles in diminished ovarian reserve.Frontiers in endocrinology · 2026Review
- Review
- GPD1L-Mediated Glycerophospholipid Metabolism Dysfunction in Women With Diminished Ovarian Reserve: Insights From Pseudotargeted Metabolomic Analysis of Follicular Fluid.Cell proliferation · 2025Article
- Non-targeted metabolomic analysis of follicular fluid in infertile individuals with poor ovarian response.Frontiers in endocrinology · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Diminished ovarian reserve (DOR) is a pathological condition characterised by reduced ovarian function, which refers to the decreased quality and quantity of oocytes, potentially causing female infertility and various health issues. Follicular fluid (FF) serves as the microenvironment for follicular development and oocyte maturation, gaining an in-depth understanding of the metabolic state of FF will help us uncover the key biological processes involved in ovarian aging, while the specific underlying pathogenic mechanisms are not fully understood. In this study, we utilised pseudotargeted metabolomic analysis of FF to reveal the glycerophospholipid metabolism dysfunction mediated by GPD1L in DOR patients. We also found that GPD1L was downregulated in granulosa cells (GCs) of DOR patients, resulting in increased cell apoptosis and mitochondrial dysfunction. Moreover, our results demonstrated that the downregulated expression of GPD1L could induce follicular atresia and impair oocyte quality in mouse ovaries. Altogether, our research suggested that GPD1L in GCs and the key metabolites in the glycerophospholipid metabolism pathway could potentially act as novel biomarkers of DOR diagnosis, paving the way for a new theoretical basis for understanding the pathogenesis of DOR.
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Registered trials
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