{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Txt":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE348nnn/GSE348247/suppl/GSE348247_gene_expression.txt.gz"],"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE348nnn/GSE348247/"]},"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=GSE348247"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Ginsenoside Rh2 Attenuates Post-Myocardial Infarction Heart Failure by Modulating the TGF-β/Smad2 Signaling Pathway","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.","dates":{"publication":"2026/09/30"},"accession":"GSE348247","cross_references":{"GSM":["GSM10069017","GSM10069016","GSM10069015","GSM10069014","GSM10069019","GSM10069018","GSM10069020","GSM10069022","GSM10069021"],"GPL":["24247"],"GSE":["348247"],"taxon":["Mus musculus"]}}