ArticleAntioxidants (Basel, Switzerland)2025
Isorhamnetin Attenuates Isoproterenol-Induced Myocardial Injury by Reducing ENO1 (Alpha-Enolase) in Cardiomyocytes.
Article in Antioxidants (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Cross-Species Identification and Validation of Hub Genes and Potential Therapeutic Targets in Myocardial Infarction.International journal of molecular sciences · 2026Article
- In Vitro Cell Viability and Migration Inhibitory Effects of Isorhamnetin in Non-Small Cell Lung Cancer Cells.Biomedicines · 2026Article
- Isorhamnetin inhibits mechanical stress-induced chondrocyte apoptosis through activation of the ROS/SRC/FOXO1 signaling pathway.Scientific reports · 2026Article
- The methylation site cg06972019 regulates the succinylation-related gene ENO1 to inhibit the occurrence of erectile dysfunction.Hereditas · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
The protective effect of isorhamnetin on myocardial injury induced by isoproterenol (ISO) was investigated to identify the key targets and pathways involved, offering potential therapeutic insights for cardiovascular diseases. A myocardial injury model was established through intraperitoneal ISO injection, and the effects of isorhamnetin on apoptosis and oxidative stress in ISO-induced myocardial injury rats were assessed. Additionally, an ISO-induced H9c2 cell injury model was established to evaluate the impact of isorhamnetin on cellular damage. The transcriptomic sequencing of H9c2 cells was conducted to identify differentially expressed genes, followed by gene enrichment analysis. Intracellular glucose, lactate, and ATP levels were quantified, and the protein expression of key pathway targets ENO1, PPARα, and PGC-1α was analyzed via immunoblotting. Isorhamnetin improved cardiac function and morphological damage, reduced serum markers of cardiac injury, and exerted cardioprotective effects by regulating oxidative stress and inhibiting apoptosis. Compared to the ISO group, the glycolytic process-with ENO1 as a key target and the PPAR signaling pathway as the core regulator-was significantly suppressed in the isorhamnetin-pretreated group. Furthermore, isorhamnetin pretreatment reduced intracellular glucose and lactate levels while increasing ATP content in a concentration-dependent manner. These findings suggest that isorhamnetin protects the heart by inhibiting ENO1, activating the PPARα/PGC-1α signaling axis, reversing isoprenaline-induced metabolic shifts in H9c2 cells, suppressing glycolysis, and enhancing ATP release, thereby mitigating apoptosis and oxidative stress.
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Registered trials
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