{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE309nnn/GSE309230/"]},"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=GSE309230"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Targeting the TNFα/TNFR1 axis to alleviate inflammation in experimental acute pancreatitis [scRNA-seq]","description":"Acute pancreatitis (AP) is an inflammatory disorder of the pancreas that can progress to systemic inflammatory response syndrome and multiple organ failure with high mortality. TNFα (tumor necrosis factor-alpha), a key proinflammatory cytokine elevated in early AP, triggers both pancreatic inflammation and acinar cell apoptosis through TNFR1 (tumor necrosis factor-alpha receptor 1) binding. However, the predominant pathological mechanism of TNFα/TNFR1 axis in AP - whether primarily mediating inflammatory responses or apoptotic pathways - remains unclear. To elucidate the precise cellular mechanisms through which Tnfr1 deficiency modulates inflammation, we employed scRNA-seq to comprehensively characterize transcriptomic alterations at single-cell resolution.","dates":{"publication":"2026/09/01"},"accession":"GSE309230","cross_references":{"GSM":["GSM9263446","GSM9263445","GSM9263444","GSM9263449","GSM9263448","GSM9263447"],"GPL":["24247"],"GSE":["309230"],"taxon":["Mus musculus"]}}