{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE301nnn/GSE301063/"]},"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=GSE301063"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Analysis by RNA-seq of the transcriptional profile of left ventricles of WT, CST-KO and CST-KO+CST treated mice","description":"Hypertension is a critical risk factor for heart failure (HF), with metabolic inflexibility playing a pivotal role. Chromogranin A (CgA)-derived peptide Catestatin (CST: hCgA352-372) exerts hypotensive and cardioprotective effects, nonetheless CST’s effect on cardiac metabolism remains unexplored. Our transcriptomic approach coupled with filtering through Boolean implication relationships identified a set of gene signatures (fibroblast, cardiomyocyte, and macrophage) that were altered in CST knockout (CST-KO) mice and restored after CST supplementation. These gene signatures obtained from our in vivo experiments corroborated with publicly available HF patient datasets.","dates":{"publication":"2026/05/01"},"accession":"GSE301063","cross_references":{"GSM":["GSM9074490","GSM9074491","GSM9074489","GSM9074485","GSM9074486","GSM9074487","GSM9074488","GSM9074492","GSM9074493","GSM9074494","GSM9074484"],"GPL":["34290"],"GSE":["301063"],"taxon":["Mus musculus"]}}