<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Txt>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE348nnn/GSE348247/suppl/GSE348247_gene_expression.txt.gz</Txt><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE348nnn/GSE348247/</Other></files><type>primary</type></body><statusCodeValue>200</statusCodeValue><statusCode>OK</statusCode></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=GSE348247</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Ginsenoside Rh2 Attenuates Post-Myocardial Infarction Heart Failure by Modulating the TGF-β/Smad2 Signaling Pathway</name><description>Background: Myocardial fibrosis and oxidative stress are key drivers of post-myocardial infarction heart failure (post-MI HF). Ginsenoside Rh2 (GRh2) has shown cardioprotective potential, but its role in post-MI HF and the underlying mechanism remain unclear. The current study aimed to investigate the therapeutic effect of GRh2 on post-MI HF and to validate its regulatory mechanism using murine, cellular, and cardiac organoid models. Methods: In vivo, Cardiac function and myocardial fibrosis were evaluated. Transcriptome analysis was performed to identify enriched signaling pathways. In vitro, H9C2 cardiomyocytes and cardiac organoids were subjected to oxygen-glucose deprivation (OGD). Cardiac injury indicators, fibrotic and oxidative stress markers, and proteins associated with the TGF-β/Smad2 pathway were measured via enzyme-linked immunosorbent assay (ELISA) and Western blotting. Results: In vivo, GRh2 treatment markedly improved cardiac function and reduced myocardial fibrosis in mice with post-MI heart failure. Transcriptomic analysis revealed that the TGF-β signaling pathway was substantially enriched. In vitro, GRh2 treatment significantly improved cell viability and reduced oxidative stress and fibrosis in OGD-exposed H9C2 cardiomyocytes and cardiac organoids. These protective effects were strongly associated with the suppression of the TGF-β/Smad2 signaling pathway. Conclusions: Ginsenoside Rh2 inhibits the TGF‑β/Smad2 signaling pathway to ameliorate cardiac dysfunction in post-MI heart failure, suggesting its potential as a therapeutic candidate.</description><dates><publication>2026/09/30</publication></dates><accession>GSE348247</accession><cross_references><GSM>GSM10069017</GSM><GSM>GSM10069016</GSM><GSM>GSM10069015</GSM><GSM>GSM10069014</GSM><GSM>GSM10069019</GSM><GSM>GSM10069018</GSM><GSM>GSM10069020</GSM><GSM>GSM10069022</GSM><GSM>GSM10069021</GSM><GPL>24247</GPL><GSE>348247</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>