ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024
Sleep Deprivation Triggers the Excessive Activation of Ovarian Primordial Follicles via β2 Adrenergic Receptor Signaling.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Slowing down the clock on ovarian aging-does the ovary hold the secret to the fountain of youth?GeroScience · 2026Review
- Sleep deprivation induces anxiety-like behaviors through IL-6 driven astrocyte-GABAergic neuron crosstalk in the PAG-ACC circuit.Journal of neuroinflammation · 2026Article
- Association of sleep duration and quality with age at natural menopause: results from NHANES 2005-2018.BMC women's health · 2026Observational
- Deconstructing the RAGE signaling maze: the molecular key to opening a new dimension of ovarian anti-aging.Experimental & molecular medicine · 2026Review
- Sleep deprivation impairs follicular development attributable to granulosa cell pyroptosis mediated by S100A8/A9-driven macrophage M1 polarization.Science advances · 2026Article
- Curcumin reduces neuroinflammation and oxidative stress in a stroke model by epigenetically regulating ADRB2 methylation through JAK2/STAT3 and Nrf2/HO-1 pathways.Journal of neuroinflammation · 2026Article
- Serine inhibits granulosa cell ferroptosis to maintain ovarian function.Nature communications · 2026Article
- Bioinformatics-based identification of glycolysis-related signatures associated with drug resistance and prognosis in lung adenocarcinoma.Frontiers in oncology · 2026Article
- Norepinephrine Induces Sertoli Cell Ferroptosis via Receptors Desensitization Causing Stress-Related Male Reproductive Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Peripheral organ crosstalk in the regulation of ovarian endocrine function and reproductive homeostasis.Life medicine · 2025Review
- Maternal sleep deprivation during pregnancy induced offspring germ cells loss through ferroptosis.Cell death discovery · 2025Article
- Single-Cell Transcriptomic Analysis of the Potential Mechanisms of Follicular Development inInternational journal of molecular sciences · 2025Article
- Impact of psychological stress on ovarian function: Insights, mechanisms and intervention strategies (Review).International journal of molecular medicine · 2025Review
- Sleep Deprivation Triggers the Excessive Activation of Ovarian Primordial Follicles via β2 Adrenergic Receptor Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
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8 authors.
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Abstract
Sleep deprivation (SD) is observed to adversely affect the reproductive health of women. However, its precise physiological mechanisms remain largely elusive. In this study, using a mouse model of SD, it is demonstrated that SD induces the depletion of ovarian primordial follicles, a phenomenon not attributed to immune-mediated attacks or sympathetic nervous system activation. Rather, the excessive secretion of stress hormones, namely norepinephrine (NE) and epinephrine (E), by overactive adrenal glands, has emerged as a key mediator. The communication pathway mediated by the KIT ligand (KITL)-KIT between granulosa cells and oocytes plays a pivotal role in primordial follicle activation. SD heightened the levels of NE/E that stimulates the activation of the KITL-KIT/PI3K and mTOR signaling cascade in an β2 adrenergic receptor (ADRB2)-dependent manner, thereby promoting primordial follicle activation and consequent primordial follicle loss in vivo. In vitro experiments further corroborate these observations, revealing that ADRB2 upregulates KITL expression in granulosa cells via the activation of the downstream cAMP/PKA pathway. Together, these results reveal the significant involvement of ADRB2 signaling in the depletion of ovarian primordial follicles under sleep-deprived conditions. Additionally, ADRB2 antagonists are proposed for the treatment or prevention of excessive activation of primordial follicles induced by SD.
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