{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE309nnn/GSE309207/"]},"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=GSE309207"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Gene expression profiling of renal tissues isolated from podocyte conditional ERRα knockin or wild-type mice injected with nephrotoxic serum","description":"Estrogen-Related Receptor Alpha (ERRα), a key member of the nuclear receptor superfamily, is well-established as a critical regulator of cellular metabolism and mitochondrial biogenesis. To investigate the functional role and molecular mechanisms of ERRα in glomerular injury, we generated podocyte-specific ERRα conditional knock-in (cKI) mice. Our studies revealed that ERRα expression was significantly upregulated in podocytes under both in vitro and in vivo injury conditions. Notably, podocyte-specific overexpression of ERRα exacerbated renal damage in mice subjected to nephrotoxic serum (NTS)-induced glomerular injury. Through comprehensive RNA-sequencing analysis, we further elucidated the underlying molecular mechanisms associated with podocyte-specific ERRα overexpression.","dates":{"publication":"2026/09/01"},"accession":"GSE309207","cross_references":{"GSM":["GSM9263138","GSM9263137","GSM9263136","GSM9263141","GSM9263140","GSM9263139"],"GPL":["23479"],"GSE":["309207"],"taxon":["Mus musculus"]}}