<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE287nnn/GSE287900/</Other></files><type>primary</type></body><statusCodeValue>200</statusCodeValue><statusCode>OK</statusCode></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE287900</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Endometrial mesenchymal stem cell derived exosomal miR-4669 promotes EMT by inducing M2 macrophage polarization via the DUSP6/ERK pathway in adenomyosis</name><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.</description><dates><publication>2026/06/30</publication></dates><accession>GSE287900</accession><cross_references><GSM>GSM8754187</GSM><GSM>GSM8754186</GSM><GSM>GSM8754185</GSM><GSM>GSM8754184</GSM><GSM>GSM8754183</GSM><GSM>GSM8754182</GSM><GPL>34284</GPL><GSE>287900</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>