{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE334nnn/GSE334095/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE334095"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Palmitate drives mitochondrial and ER stress through disruption of the CD73-Adenosine axis","description":"Bulk RNA sequencing was used to characterize transcriptional changes associated with the dysfunctional metabolic state in murine gingival fibroblasts (mGF). The mGF were treated with BSA control, palmitate, IL-1β, or palmitate plus IL-1β. Gene ontology analysis demonstrated enrichment of pathways related to innate immune activation, oxidative stress, mitochondrial dysfunction, ER stress, and purine metabolism. Palmitate disrupts the Cd73-adenosine axis while promoting mitochondrial dysfunction, oxidative stress, and Perk-mediated ER stress in gingival fibroblasts. Adenosine signaling protects against lipotoxic-induced ER stress, highlighting the relevance of the Cd73-adenosine pathway for metabolic and inflammatory diseases.","dates":{"publication":"2026/07/08"},"accession":"GSE334095","cross_references":{"GSM":["GSM9780661","GSM9780650","GSM9780651","GSM9780660","GSM9780654","GSM9780655","GSM9780652","GSM9780653","GSM9780658","GSM9780647","GSM9780659","GSM9780648","GSM9780656","GSM9780646","GSM9780657","GSM9780649"],"GPL":["24247"],"GSE":["334095"],"taxon":["Mus musculus"]}}