{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE244nnn/GSE244596/"]},"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=GSE244596"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Dysregulated gene expression in human rheumatoid arthritis-associated interstitial lung disease(RA-ILD) and rheumatoid arthritis (RA) peripheral blood samples","description":"RA-associated interstitial lung disease (RA-ILD) is an increasingly recognized extra-articular manifestations (EAMs) in the RA, with highly morbidity and mortality. Due to the etiology of RA-ILD is unknown, we collected peripheral blood samples of RA-ILD and RA patients. Differential gene expression analysis was employed to identify key genes, common pathways, and potential drug targets for RA-ILD. Furthermore, RT-qPCR was conducted to verify potential biomarkers in RA-ILD.This study was undertaken to understand the disease's molecular basis better and provide relevant insight into phenotypical alterations and mechanisms involved in RA-ILD pathogenesis.","dates":{"publication":"2026/10/01"},"accession":"GSE244596","cross_references":{"GSM":["GSM7821525","GSM7821533","GSM7821534","GSM7821531","GSM7821532","GSM7821530","GSM7821528","GSM7821529","GSM7821526","GSM7821527"],"GPL":["30209"],"GSE":["244596"],"taxon":["Homo sapiens"]}}