<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/GSE306nnn/GSE306887/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></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=GSE306887</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>FABP4 Contributes to Preeclampsia Through Dysregulating Lipid Metabolism and Inducing Mitochondrial Oxidative Stress in Trophoblasts</name><description>Preeclampsia (PE) is a pregnancy-specific hypertensive disorder characterized by abnormal placental development and systemic endothelial dysfunction. Previous studies have suggested that fatty acid binding protein 4 (FABP4) is involved in lipid metabolism and oxidative stress regulation in various metabolic and cardiovascular diseases. However, its specific role and underlying mechanisms in PE, particularly in trophoblast function and mitochondrial homeostasis, remain unclear. This study aims to investigate the role of FABP4 in the pathogenesis of PE by exploring its effects on trophoblast cell function and mitochondrial oxidative stress through regulating lipid metabolism.</description><dates><publication>2026/03/25</publication></dates><accession>GSE306887</accession><cross_references><GSM>GSM9211700</GSM><GSM>GSM9211699</GSM><GSM>GSM9211698</GSM><GSM>GSM9211697</GSM><GSM>GSM9211696</GSM><GSM>GSM9211695</GSM><GPL>24676</GPL><GSE>306887</GSE><taxon>Homo sapiens</taxon><PMID>[41664057]</PMID></cross_references></HashMap>