{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE287nnn/GSE287900/"]},"type":"primary"},"statusCodeValue":200,"statusCode":"OK"}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE287900"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Endometrial mesenchymal stem cell derived exosomal miR-4669 promotes EMT by inducing M2 macrophage polarization via the DUSP6/ERK pathway in adenomyosis","description":"Adenomyosis-associated macrophage (AAM) polarization-induced epithelial‐mesenchymal transition (EMT) has been implicated as a key driver in AM progression. Mechanistic studies revealed that miR-4669 induces M2 macrophage polarization by directly downregulating DUSP6 expression and activating the MAPK/ERK pathway. In turn, the polarized M2 macrophages promote EMT in ISK cells via TGF-β1 secretion. In vivo studies demonstrated that miR-4669 depletion inhibits EECs invasion and migration by targeting the DUSP6/ERK1/2 pathway in macrophages.","dates":{"publication":"2026/06/30"},"accession":"GSE287900","cross_references":{"GSM":["GSM8754187","GSM8754186","GSM8754185","GSM8754184","GSM8754183","GSM8754182"],"GPL":["34284"],"GSE":["287900"],"taxon":["Homo sapiens"]}}