<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/GSE322nnn/GSE322779/</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=GSE322779</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Transcription factor TFEB antagonizes cardiac hypertrophy and failure by enhancing lysosomal capacity and mitochondrial function</name><description>Pathological cardiac remodeling and increased afterload-driven demand contribute to heart failure. TFEB is a key regulator of lysosomal genes and mitochondrial function and is activated in response to external stress. To elucidate TFEB-dependent transcriptional programs under hypertrophic stress, we profiled left ventricular transcriptomes from a cardiomyocyte-specific TFEB knockout mouse model subjected to transverse aortic constriction (TAC) or sham surgery, with wild-type littermate controls, followed by downstream multi-omics integration.</description><dates><publication>2026/05/11</publication></dates><accession>GSE322779</accession><cross_references><GSM>GSM9558311</GSM><GSM>GSM9558310</GSM><GSM>GSM9558313</GSM><GSM>GSM9558302</GSM><GSM>GSM9558312</GSM><GSM>GSM9558315</GSM><GSM>GSM9558304</GSM><GSM>GSM9558303</GSM><GSM>GSM9558314</GSM><GSM>GSM9558306</GSM><GSM>GSM9558317</GSM><GSM>GSM9558316</GSM><GSM>GSM9558305</GSM><GSM>GSM9558308</GSM><GSM>GSM9558307</GSM><GSM>GSM9558309</GSM><GPL>24247</GPL><GSE>322779</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>