ArticleCellular and molecular life sciences : CMLS2025
Aminophylline targets miR-128-3p/Slc7a11 axis to attenuate neuronal ferroptosis after traumatic brain injury.
Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Traumatic brain injury-related ferroptosis: current perspectives.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Review
- A novel antibacterial hydrogel containing aminophylline as a versatile platform for neural differentiation of hWJMSCs through the CREB pathway.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Traumatic brain injury (TBI) is a significant global health issue, characterized by high rates of morbidity and mortality, along with substantial economic strains on healthcare systems. This study explores the potential of Aminophylline (AMP), a medication traditionally used for cardiovascular conditions and bronchiectasis, to enhance TBI outcomes by protecting against neuronal damage. Our findings indicate that AMP treatment significantly reduces neuronal ferroptosis in the cortex, leading to less tissue damage and notable improvements in cognitive and motor functions in mice subjected to controlled cortical impact (CCI). Additionally, we found that TBI resulted in decreased expression of miR-128-3p, a reduction that was further strengthened by AMP treatment. Gain-of-function experiments showed that overexpressing miR-128-3p increases neuronal ferroptosis by targeting Slc7a11, indicating how AMP mitigates cognitive and motor impairments in CCI mice. This study highlights the potential of AMP in treating TBI through the miR-128-3p/Slc7a11 pathway, marking the first report of its protective effects against ferroptosis in TBI.
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Registered trials
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