ArticleMolecular human reproduction2024
Cellular senescence of granulosa cells in the pathogenesis of polycystic ovary syndrome.
Article in Molecular human reproduction, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Multi-ancestry genome-wide association analyses of polycystic ovary syndrome.Nature genetics · 2025Pooled it
- A Biological Disease-Staging Model of Polyendocrine Metabolic Ovarian Syndrome: From Plasticity-Dominant States to Pathological Remodeling.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Long-term sucralose exposure might possibly contribute to the formation of polycystic ovaries by promoting ovarian senescence in animal models.Human cell · 2026Article
- Single‑cell atlas reveals a Wilms' tumor 1‑mediated axis driving granulosa cell senescence in human ovarian aging.International journal of molecular medicine · 2026Article
- Reprogramming senescent granulosa cells for germ-cell generation.Science China. Life sciences · 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
- Deconstructing the RAGE signaling maze: the molecular key to opening a new dimension of ovarian anti-aging.Experimental & molecular medicine · 2026Review
- Jiawei Zaoqi Decoction Attenuates Polycystic Ovary Syndrome by Inhibiting AGE-RAGE-Mediated Cell Senescence of Granulosa Cells.Current pharmaceutical design · 2026Article
- Cellular senescence and polycystic ovary syndrome: mechanisms and therapeutic strategies from a new perspective.Annals of medicine · 2025Review
- Oxidative Stress-Telomere Axis in IVF: Molecular Mechanisms, Biomarkers, and Clinical Translation.International journal of molecular sciences · 2025Review
- Granulosa cell RNA-Seq insights into senescence and sphingolipid metabolism disorder in PCOS: aspirin as a potential therapeutic drug.Reproductive biology and endocrinology : RB&E · 2025Article
- Rubicon, a Key Molecule for Oxidative Stress-Mediated DNA Damage, in Ovarian Granulosa Cells.Antioxidants (Basel, Switzerland) · 2025Article
Corrections and comments
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders in women of reproductive age, but its pathology has not been fully characterized and the optimal treatment strategy remains unclear. Cellular senescence is a permanent state of cell-cycle arrest that can be induced by multiple stresses. Senescent cells contribute to the pathogenesis of various diseases, owing to an alteration in secretory profile, termed 'senescence-associated secretory phenotype' (SASP), including with respect to pro-inflammatory cytokines. Senolytics, a class of drugs that selectively eliminate senescent cells, are now being used clinically, and a combination of dasatinib and quercetin (DQ) has been extensively used as a senolytic. We aimed to investigate whether cellular senescence is involved in the pathology of PCOS and whether DQ treatment has beneficial effects in patients with PCOS. We obtained ovaries from patients with or without PCOS, and established a mouse model of PCOS by injecting dehydroepiandrosterone. The expression of the senescence markers p16INK4a, p21, p53, γH2AX, and senescence-associated β-galactosidase and the SASP-related factor interleukin-6 was significantly higher in the ovaries of patients with PCOS and PCOS mice than in controls. To evaluate the effects of hyperandrogenism and DQ on cellular senescence in vitro, we stimulated cultured human granulosa cells (GCs) with testosterone and treated them with DQ. The expression of markers of senescence and a SASP-related factor was increased by testosterone, and DQ reduced this increase. DQ reduced the expression of markers of senescence and a SASP-related factor in the ovaries of PCOS mice and improved their morphology. These results indicate that cellular senescence occurs in PCOS. Hyperandrogenism causes cellular senescence in GCs in PCOS, and senolytic treatment reduces the accumulation of senescent GCs and improves ovarian morphology under hyperandrogenism. Thus, DQ might represent a novel therapy for PCOS.
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