{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE319nnn/GSE319606/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"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=GSE319606"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Effect of depletion of NAMPT in human endothelial cells (B4G12)","description":"In our study, NAMPT was found downregulated In the corneal endothelium of patients with Fuchs endothelial corneal dystrophy. In this study, NAMPT was knocked down in the human corneal endothelial cell line (B4G12), and significant decreases in corneal endothelial cell viability, as well as the activation of immune-related pathways and extracellular matrix remodeling pathways, were observed. These changes are consistent with the expression profile of corneal endothelium in FECD patients, suggesting that downregulation of NAMPT plays an important role in the pathogenesis of FECD.","dates":{"publication":"2026/06/10"},"accession":"GSE319606","cross_references":{"GSM":["GSM9521140","GSM9521141","GSM9521136","GSM9521137","GSM9521138","GSM9521139"],"GPL":["24676"],"GSE":["319606"],"taxon":["Homo sapiens"],"PMID":["[42206947]"]}}