ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Morusin attenuates myocardial ischemia/reperfusion injury by inhibiting ferroptosis via dual activation of the Nrf2/HO-1 pathway and mTORC1-dependent GPX4 synthesis.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- Research Progress on Anti-Inflammatory Adipokine SFRP5-Mediated Lipid Metabolism and Its Potential Role in Neural Development.Immunity, inflammation and disease · 2026Pooled it
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial ischemia/reperfusion injury (MIRI) involves exacerbated oxidative stress and ferroptosis, a regulated cell death driven by iron-dependent lipid peroxidation. Morusin, a flavonoid from Morus alba, exhibits antioxidant properties, but its role in MIRI remains unclear. This study investigated morusin's cardioprotective effects and mechanisms in in vitro and in vivo MIRI models. In oxygen-glucose deprivation/reoxygenation (OGD/R)-treated H9c2 cells and murine I/R injury models, morusin significantly improved cell viability, reduced oxidative stress markers (ROS, MDA, 4-HNE), and suppressed inflammatory cytokine release. Mechanistically, morusin stabilized nuclear factor erythroid 2-related factor 2 (Nrf2) by disrupting its interaction with Keap1, thereby activating the Nrf2/HO-1 antioxidant axis. This activation enhanced glutathione peroxidase 4 (GPX4) transcription, a key ferroptosis suppressor. Additionally, morusin promoted GPX4 protein synthesis via mTORC1 signaling, evidenced by increased phosphorylation of S6K and 4EBP1. Genetic or pharmacological inhibition of Nrf2, HO-1, or mTORC1 abolished morusin's protective effects, confirming their critical roles. In vivo, morusin reduced myocardial infarct size, preserved mitochondrial integrity, and lowered serum cardiac injury markers (LDH, CK-MB) in I/R mice. These findings reveal that morusin mitigates MIRI by dual modulation of ferroptosis through Nrf2/HO-1-mediated antioxidative responses and mTORC1-dependent GPX4 upregulation. This study highlights morusin's therapeutic potential for ischemic heart diseases, offering novel insights into targeting ferroptosis for cardioprotection.
Indexed as
Identifiers
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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 OpenQuestion graph.