Dataset Information

Ginsenoside Rh2 Attenuates Post-Myocardial Infarction Heart Failure by Modulating the TGF-β/Smad2 Signaling Pathway

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE348247 | GEO | 2026/09/30

REPOSITORIES: GEO

ACCESS DATA

Dataset's files

Source:

			Action	DRS
		Other
	GSE348247_gene_expression.txt.gz	Txt

Items per page:

1 - 2 of 2

Similar Datasets

Project description:Background: Postmenopausal women have higher risks of myocardial infarction (MI) and subsequent cardiac dysfunction. Exercise is widely recognized to protect the cardiovascular system, but its molecular mechanisms in postmenopausal MI remain not fully understood. This study explored the effects and mechanism of swimming exercise against cardiac dysfunction in ovariectomized (OVX) mice post-MI. Methods: OVX mice were subjected to a 3-week swimming training before MI induction via permanent ligation of left anterior descending artery. Cardiac systolic function was evaluated by echocardiography. Masson, HE, WGA staining, RT-qPCR, and Western blotting were combined to detect the extent of cardiomyocyte hypertrophy, myocardial fibrosis, and apoptosis. To explore the key exercise-effectors, we detected microRNAs (miR-21, miR-146a, miR-155) in serum samples of elderly post-MI women subsequent to exercise rehabilitation training. miR-21 expression was further investigated in heart sample of OVX plus MI mice. The role of miR-21 in vivo was elucidated through miR-21 knockout mice model and AAV9-mediated miR-21 overexpression mice model. The function of miR-21 in vitro were evaluated in cardiac fibroblasts isolated from OVX mice and treated with TGF-β to induce its activation. miR-21 targets were revealed by microarray analysis and verified by luciferase reporter and functional rescue assays. Results: Swimming significantly improved cardiac function in OVX mice post-MI, alleviated cardiomyocyte hypertrophy, reduced myocardial fibrosis, and inhibited apoptosis. miR-21 expression was downregulated by exercise training both in heart of OVX mice post-MI and in serum of elderly women after MI. miR-21 knockout mimicked swimming’s cardioprotective effects towards OVX mice post-MI, while miR-21 overexpression abolished these effects. The overexpression of miR-21 promoted the TGF-β-induced differentiation of cardiac fibroblasts into myofibroblasts and their proliferation, whereas its inhibition blocked TGF-β’s pro-fibrotic role. Microarray analysis and luciferase assays identified Sox7 as a direct miR-21 target, and Sox7 knockdown reversed anti-fibrotic effect of inhibiting miR-21. Conclusion: Swimming protects against post-MI cardiac dysfunction in OVX mice by downregulating myocardial miR-21, thereby upregulating its target gene Sox7 and inhibiting cardiac fibroblast activation. miR-21 and its downstream target Sox7 contributes to cardioprotective effects of swimming, offering a potential target for postmenopausal MI treatment.

Dataset Information

Ginsenoside Rh2 Attenuates Post-Myocardial Infarction Heart Failure by Modulating the TGF-β/Smad2 Signaling Pathway

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets