<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/GSE335nnn/GSE335813/</Other></files><type>primary</type></body><statusCodeValue>200</statusCodeValue><statusCode>OK</statusCode></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</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=GSE335813</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Transcriptomic effects of neprilysin inhibition during endothelin-1–induced hypertrophic stress in human iPSC-derived cardiomyocytes</name><description>Human induced pluripotent stem cell–derived cardiomyocytes were used to investigate the cardiomyocyte-intrinsic effects of neprilysin inhibition during hypertrophic stress. Cardiomyocytes were treated with endothelin-1, the neprilysin inhibitor sacubitrilat, a combination of endothelin-1 and sacubitrilat, or vehicle control. Bulk RNA sequencing was performed to characterize transcriptional remodeling induced by endothelin-1 and to determine whether neprilysin inhibition modifies this response.</description><dates><publication>2026/06/22</publication></dates><accession>GSE335813</accession><cross_references><GSM>GSM9821574</GSM><GSM>GSM9821573</GSM><GSM>GSM9821572</GSM><GSM>GSM9821571</GSM><GSM>GSM9821578</GSM><GSM>GSM9821577</GSM><GSM>GSM9821576</GSM><GSM>GSM9821575</GSM><GSM>GSM9821579</GSM><GSM>GSM9821570</GSM><GSM>GSM9821581</GSM><GSM>GSM9821580</GSM><GPL>34284</GPL><GSE>335813</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>