ArticleCombinatorial chemistry & high throughput screening2026
Ferroptosis-related Biotargets and Network Mechanisms of Maslinic Acid Against Myocardial Ischemia-reperfusion Injury: An Integrated Bioinformatic and Experimental Approach.
Article in Combinatorial chemistry & high throughput screening, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Role of maslinic acid in ischemia-reperfusion-induced testicular injury in rats.Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES · 2026Article
- The interaction between ferroptosis and myocardial ischemia-reperfusion injury: molecular mechanisms and potential therapeutic targets.European journal of medical research · 2025Review
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Authors and funding
8 authors.
Funding
Abstract
backgroundMaslinic acid (MA), a pentacyclic triterpenoid compound derived from leaves and fruits of Olea europaea, bears multi-pharmacological properties. Our previous studies found that MA exerted a cardioprotective effect by modulating oxidative stress, inflammation, and apoptosis during myocardial ischemia-reperfusion injury (MIRI). Nevertheless, data regarding the anti-ferroptosis effects of MA on MI/RI remains unidentified. AIMS AND SCOPE: This study aimed to explore the effects of MA on ferroptosis induced by MI/RI, with a focus on elucidating the underlying mechanisms through an integrated approach of network pharmacology and experimental validation. MATERIALS AND
methodsSeveral public databases and a protein-protein interaction (PPI) network were used to identify the core targets shared by MI/RI, ferroptosis, and MA. The molecular function, cell component, biological process, and potential signaling pathways of core genes were analyzed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment. Subsequently, molecular docking and in vitro experiments were carried out to further validate network pharmacology results.
resultsA total of 21 unique intersection genes were obtained as potential targets of MA in treating MI/RI-induced ferroptosis. The 10 hub genes with the highest interaction scores were identified from PPI analysis. GO and KEGG enrichment showed the contribution of the core genes to pharmacological actions and mechanisms in MA treatment of MI/RI, especially the ferroptosis- related signaling pathways. Additionally, MA docked well with ranked core targets, including MAPK, MTOR, STAT3, PTGS2, and MDM2. Subsequently, in vitro experiments revealed that MA notably alleviated oxidative damage, reduced ferrous iron overload and ferroptosis, and regulated the expression of ferroptosis-related genes (GPX4, PTGS2, and ACSL4) in erastin-induced H9c2 cells. Meanwhile, MA could significantly reduce phosphorylation of MAPK (ERK1/2) levels in H9c2 cells.
conclusionBy utilizing network pharmacology and experimental data, our study revealed the correlation between MA and ferroptosis following MI/RI, and concluded that MA might protect against MI/RI by reducing ferroptosis through the ERK1/2 signaling pathway. This finding offered fresh insights into the pharmacological mechanisms of MA against MI/RI.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.