ArticlePeerJ2024
Gypenosides exert cardioprotective effects by promoting mitophagy and activating PI3K/Akt/GSK-3
Article in PeerJ, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Role of the PI3K/AKT signaling pathway in regulating gene expression in rheumatoid arthritis (Review).Molecular medicine reports · 2026Review
- Gypenoside XLIX and Mitochondria-Associated ER Membranes in Non-Alcoholic Fatty Liver Disease: Mechanistic Insights and Emerging Perspectives.Molecules (Basel, Switzerland) · 2026Review
- Research progress on targeting autophagy pathways with medicinal plants and their active metabolites for the treatment of heart failure.Frontiers in pharmacology · 2026Review
- Protective effects of gypenosides on LDL-induced myocardial injury through the miR-223/NLRP3 axis in hyperlipidemia.Frontiers in nutrition · 2026Article
- Therapeutic Potential ofPharmaceuticals (Basel, Switzerland) · 2025Article
- PINK1 overexpression suppresses p38 MAPK/NF‑κB signaling to attenuate chondrocyte senescence in osteoarthritis.International journal of molecular medicine · 2025Article
- From Gut to Heart: Targeting Trimethylamine N-Oxide as a Novel Strategy in Heart Failure Management.Biomolecules · 2025Review
- Alleviation of Gypenosides on Peripheral and Central Fatigue via Anti-Inflammation, Anti-Oxidation and Neurotransmitter Regulation.Food science & nutrition · 2025Article
- Elucidating the Molecular Mechanisms of Hederagenin-Regulated Mitophagy in Cervical Cancer SiHa Cells through an Integrative Approach Combining Proteomics and Advanced Network Association Algorithm.Journal of proteome research · 2025Article
- Identification of mitochondria-related genes associated with anesthetics in patients undergoing off-pump coronary artery bypass grafting surgery.Frontiers in surgery · 2025Article
- Mitochondrial fission process 1 protein: a comprehensive review of its core roles in mitochondrial dynamics, disease, and therapeutic targets.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Background: Methods: The bioactive components in GYPs and the potential targets in treating HF were obtained and screened using the network pharmacology approach, followed by drug-disease target prediction and enrichment analyses. The pharmacological effects of GYPs in cardioprotection, mitochondrial function, mitochondrial quality control, and underlying mechanisms were further investigated in Doxorubicin (Dox)-stimulated H9c2 cardiomyocytes. Results: A total of 88 bioactive compounds of GYPs and their respective 71 drug-disease targets were identified. The hub targets covered MAPK, EGFR, PI3KCA, and Mcl-1. Enrichment analysis revealed that the pathways primarily contained PI3K/Akt, MAPK, and FoxO signalings, as well as calcium regulation, protein phosphorylation, apoptosis, and mitophagy process. In Dox-stimulated H9c2 rat cardiomyocytes, pretreatment with GYPs increased cell viability, enhanced cellular ATP content, restored basal oxygen consumption rate (OCR), and improved mitochondrial membrane potential (MMP). Furthermore, GYPs improved PINK1/parkin-mediated mitophagy without influencing mitochondrial fission/fusion proteins and the autophagic LC3 levels. Mechanistically, the phosphorylation of PI3K, Akt, GSK-3β, and the protein level of Mcl-1 was upregulated by GYP treatment. Conclusion: Our findings reveal that GYPs exert cardioprotective effects by rescuing the defective mitophagy, and PI3K/Akt/GSK-3
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Registered trials
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