ArticleeLife2022
Metformin abrogates pathological TNF-α-producing B cells through mTOR-dependent metabolic reprogramming in polycystic ovary syndrome.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Therapeutic Potential of Anti-Obesity Drugs in Obesity-Associated Female Reproductive Dysfunction: Translating Mechanistic Evidence into Personalized Clinical Strategies.Medicina (Kaunas, Lithuania) · 2026Review
- CDH4/UBA1/RBMX axis promotes polycystic ovary syndrome progression through YAP1 activation.Cellular & molecular biology letters · 2026Article
- Analysis of the association between cytokine expression in the endometrial microenvironment and insulin resistance in polycystic ovary syndrome.Endocrine · 2026Article
- Beyond glycemic control: molecular mechanisms of metformin in modulating cytokine networks in polycystic ovary syndrome.Frontiers in endocrinology · 2026Review
- Ameliorating effects of bromelain with or without metformin on endocrine-metabolic disturbances in letrozole-induced polycystic ovary syndrome in female rats via targeting SIRT1, insulin resistance, and inflammatory axis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Metformin facilitates osteogenic differentiation of bone marrow stromal cells through AMPK-dependent autophagy: an investigation into the healing of osteoporotic fractures in murine models.Journal of orthopaedic surgery and research · 2025Article
- Feedback regulation of VISTA and Treg by TNF-α controls T cell responses in drug allergy.Allergy · 2025Article
- Metformin Enhances the Chemosensitivity of Gastric Cancer to Cisplatin by Downregulating Nrf2 Level.Analytical cellular pathology (Amsterdam) · 2025Article
- Loureirin B Reduces Insulin Resistance and Chronic Inflammation in a Rat Model of Polycystic Ovary Syndrome by Upregulating GPR120 and Activating the LKB1/AMPK Signaling Pathway.International journal of molecular sciences · 2024Article
- Cross-talk between oxidative stress and lipid metabolism regulators reveals molecular clusters and immunological characterization in polycystic ovarian syndrome.Lipids in health and disease · 2024Article
- Bushenhuoluo Decoction improves polycystic ovary syndrome by regulating exosomal miR-30a-5p/ SOCS3/mTOR/NLRP3 signaling-mediated autophagy and pyroptosis.Journal of ovarian research · 2024Article
- Systematic low-grade chronic inflammation and intrinsic mechanisms in polycystic ovary syndrome.Frontiers in immunology · 2024Review
- Multi-omics approach to reveal follicular metabolic changes and their effects on oocyte competence in PCOS patients.Frontiers in endocrinology · 2024Article
- Abnormal Expression of Prolyl Oligopeptidase (POP) and Its Catalytic Products Ac-SDKP Contributes to the Ovarian Fibrosis Change in Polycystic Ovary Syndrome (PCOS) Mice.Biomedicines · 2023Article
- Article
- Immunometabolic Signature during Respiratory Viral Infection: A Potential Target for Host-Directed Therapies.Viruses · 2023Review
- A novel model based on necroptosis to assess progression for polycystic ovary syndrome and identification of potential therapeutic drugs.Frontiers in endocrinology · 2023Article
- The Role and Mechanism of Metformin in Inflammatory Diseases.Journal of inflammation research · 2023Review
- Posttranslational modifications in pathogenesis of PCOS.Frontiers in endocrinology · 2022Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
B cells contribute to the pathogenesis of polycystic ovary syndrome (PCOS). Clinically, metformin is used to treat PCOS, but it is unclear whether metformin exerts its therapeutic effect by regulating B cells. Here, we showed that the expression level of tumor necrosis factor-alpha (TNF-α) in peripheral blood B cells from PCOS patients was increased. Metformin used in vitro and in vivo was able to reduce the production of TNF-α in B cells from PCOS patients. Administration of metformin improved mouse PCOS phenotypes induced by dehydroepiandrosterone (DHEA) and also inhibited TNF-α expression in splenic B cells. Furthermore, metformin induced metabolic reprogramming of B cells in PCOS patients, including the alteration in mitochondrial morphology, the decrease in mitochondrial membrane potential, Reactive Oxygen Species (ROS) production and glucose uptake. In DHEA-induced mouse PCOS model, metformin altered metabolic intermediates in splenic B cells. Moreover, the inhibition of TNF-α expression and metabolic reprogramming in B cells of PCOS patients and mouse model by metformin were associated with decreased mTOR phosphorylation. Together, TNF-α-producing B cells are involved in the pathogenesis of PCOS, and metformin inhibits mTOR phosphorylation and affects metabolic reprogramming, thereby inhibiting TNF-α expression in B cells, which may be a new mechanism of metformin in the treatment of PCOS.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.