ArticleScientific reports2025
Esculetin inhibits ferroptosis after ICH by promoting NUDT1-mediated m7G methylation modification of GPX4.
Article in Scientific reports, 2025. 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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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
2 citing papers in PubMed.
- Esculetin and its derivatives: recent advances in efficacy, mechanisms, and translational challenges.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Fraxini cortex (Qinpi): reframing a traditional heat-clearing botanical drug as a systemic immune-metabolic regulator.Frontiers in pharmacology · 2026Review
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Authors and funding
5 authors.
Funding
Abstract
Intracerebral hemorrhage (ICH) is the most morbid of all stroke types with a high mortality and significant disability burden. Inhibiting ferroptosis after ICH will effectively treat ICH and improve prognosis. Esculetin is the main active ingredient of the Chinese medicine Cortex Fraxini, which has neuroprotective effects. 7-methylguanosine (m7G) methylation is a common RNA modification that regulates mRNA stability and translation, playing an important role in neural development and function, as well as in ferroptosis-related pathways. In this study, we used hemin-induced PC12 cells to investigate the impact of esculetin on ferroptosis and the involvement of m7G modification. Cell viability was measured by cell counting kit-8. Cell death was evaluated by measuring the levels of LDH release and PI-positive cells. Ferroptosis was assessed by measuring the levels of Fe
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