<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE301nnn/GSE301063/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE301063</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Analysis by RNA-seq of the transcriptional profile of left ventricles of WT, CST-KO and CST-KO+CST treated mice</name><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.</description><dates><publication>2026/05/01</publication></dates><accession>GSE301063</accession><cross_references><GSM>GSM9074490</GSM><GSM>GSM9074491</GSM><GSM>GSM9074489</GSM><GSM>GSM9074485</GSM><GSM>GSM9074486</GSM><GSM>GSM9074487</GSM><GSM>GSM9074488</GSM><GSM>GSM9074492</GSM><GSM>GSM9074493</GSM><GSM>GSM9074494</GSM><GSM>GSM9074484</GSM><GPL>34290</GPL><GSE>301063</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>