{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Isola JVV"],"funding":["Global Consortium for Reproductive Longevity and Equality - GCRLE-4501","NIA NIH HHS","U.S. Department of Health & Human Services | NIH | National Institute on Aging","ODCDC CDC HHS","Global Consortium for Reproductive Longevity and Equality - GCRLE-0523","U.S. Department of Health & Human Services | NIH | NIH Office of the Director","Presbyterian Health Foundation","NIH HHS"],"pagination":["145-162"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10798902"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["4(1)"],"pubmed_abstract":["Ovarian aging leads to diminished fertility, dysregulated endocrine signaling and increased chronic disease burden. These effects begin to emerge long before follicular exhaustion. Female humans experience a sharp decline in fertility around 35 years of age, which corresponds to declines in oocyte quality. Despite a growing body of work, the field lacks a comprehensive cellular map of the transcriptomic changes in the aging mouse ovary to identify early drivers of ovarian decline. To fill this gap we performed single-cell RNA sequencing on ovarian tissue from young (3-month-old) and reproductively aged (9-month-old) mice. Our analysis revealed a doubling of immune cells in the aged ovary, with lymphocyte proportions increasing the most, which was confirmed by flow cytometry. We also found an age-related downregulation of collagenase pathways in stromal fibroblasts, which corresponds to rises in ovarian fibrosis. Follicular cells displayed stress-response, immunogenic and fibrotic signaling pathway inductions with aging. This report provides critical insights into mechanisms responsible for ovarian aging phenotypes. The data can be explored interactively via a Shiny-based web application."],"journal":["Nature aging"],"pubmed_title":["A single-cell atlas of the aging mouse ovary."],"pmcid":["PMC10798902"],"funding_grant_id":["P30 AG050911","Pilot Funding","S10 OD028479","R01 AG069742"],"pubmed_authors":["Ocanas SR","Isola JVV","Ko S","Kovats S","Alberola-Ila J","Hense JD","Carter HNC","Schneider A","Mondal SA","Freeman WM","Stout MB","Hubbart CR"],"additional_accession":[]},"is_claimable":false,"name":"A single-cell atlas of the aging mouse ovary.","description":"Ovarian aging leads to diminished fertility, dysregulated endocrine signaling and increased chronic disease burden. These effects begin to emerge long before follicular exhaustion. Female humans experience a sharp decline in fertility around 35 years of age, which corresponds to declines in oocyte quality. Despite a growing body of work, the field lacks a comprehensive cellular map of the transcriptomic changes in the aging mouse ovary to identify early drivers of ovarian decline. To fill this gap we performed single-cell RNA sequencing on ovarian tissue from young (3-month-old) and reproductively aged (9-month-old) mice. Our analysis revealed a doubling of immune cells in the aged ovary, with lymphocyte proportions increasing the most, which was confirmed by flow cytometry. We also found an age-related downregulation of collagenase pathways in stromal fibroblasts, which corresponds to rises in ovarian fibrosis. Follicular cells displayed stress-response, immunogenic and fibrotic signaling pathway inductions with aging. This report provides critical insights into mechanisms responsible for ovarian aging phenotypes. The data can be explored interactively via a Shiny-based web application.","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jan","modification":"2026-03-27T16:37:19.794Z","creation":"2025-04-04T19:21:35.549Z"},"accession":"S-EPMC10798902","cross_references":{"pubmed":["38200272"],"doi":["10.1038/s43587-023-00552-5"]}}