ArticleJournal of translational medicine2026
LSD1 maintains oocyte quality by epigenetically repressing CAMK2β to control granulosa cell-oocyte communication.
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPoor ovarian response (POR) is a major challenge in assisted reproduction, yet its molecular basis remains poorly understood. Communication between granulosa cells (GCs) and oocytes is critical for folliculogenesis, but how it is regulated epigenetically is unclear.
methodsWe generated granulosa cell-specific Lsd1 knockout mice. Human GCs from POR patients (classified by Poseidon criteria) and controls were analyzed. Mechanistic studies employed RNA-seq, ChIP-seq, TEM, calcium imaging, and actin polymerization assays. LSD1 was knocked out in KGN cells via CRISPR/Cas9.
resultsLSD1 was significantly downregulated in GCs of POR patients. Its loss in mice recapitulated the POR phenotype: reduced fertility, low estrogen levels, impaired antral follicle formation, poor response to gonadotropins, and defective oocytes with meiotic and spindle abnormalities. Mechanistically, Lsd1 deficiency increased H3K4me2 enrichment at the Camk2β promoter, elevating CAMK2β expression. This led to elevated cytoplasmic Ca
conclusionsOur findings reveal that GC LSD1 epigenetically represses Camk2β to maintain calcium signaling, actin dynamics, and TZPs integrity, thereby ensuring functional GC-oocyte communication and oocyte competence. Downregulation of LSD1 and upregulation of CAMK2β in GCs is a hallmark of POR, identifying this pathway as a potential diagnostic biomarker and therapeutic target. CAMK2β inhibition represents a promising strategy for treating ovarian dysfunction.
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