{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["24(1)"],"submitter":["Zhang J"],"pubmed_abstract":["<h4>Background</h4>Poor 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.<h4>Methods</h4>We 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.<h4>Results</h4>LSD1 was significantly downregulated in GCs of POR patients. Its loss in mice recapitulated the POR phenotype: reduced fertility, low estrogen levels, impaired antral follicle formati"],"journal":["Journal of translational medicine"],"pagination":["284"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12924375"],"repository":["biostudies-literature"],"pubmed_title":["LSD1 maintains oocyte quality by epigenetically repressing CAMK2β to control granulosa cell-oocyte communication."],"pmcid":["PMC12924375"],"pubmed_authors":["Sheng Z","Zhang T","Zhu Z","Zhang J","Hu Z","Zhang H","He M","Yu Y"],"additional_accession":[]},"is_claimable":false,"name":"LSD1 maintains oocyte quality by epigenetically repressing CAMK2β to control granulosa cell-oocyte communication.","description":"<h4>Background</h4>Poor 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.<h4>Methods</h4>We 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.<h4>Results</h4>LSD1 was significantly downregulated in GCs of POR patients. Its loss in mice recapitulated the POR phenotype: reduced fertility, low estrogen levels, impaired antral follicle formati","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Jan","modification":"2026-07-16T15:13:33.235Z","creation":"2026-07-10T03:09:21.459Z"},"accession":"S-EPMC12924375","cross_references":{"pubmed":["41593739"],"doi":["10.1186/s12967-026-07730-0"]}}