ArticleInternational journal of biological sciences2025
The Neuroprotective Effects of Caffeine in a Neonatal Hypoxia-Ischemia Model are Regulated through the AMPK/mTOR Pathway.
Article in International journal of biological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- NLRP3 Regulation in Neonatal Hypoxic-Ischemic Encephalopathy-Focus on Microglial Activation.International journal of molecular sciences · 2026Article
- Article
- The role of persistent inflammation in failed recovery after perinatal brain injury: is resolution the cure?Journal of neuroinflammation · 2026Review
- Caffeine as a Treatment for Perinatal Hypoxic-Ischemic Brain Injury: The Potential Risks and Benefits.Developmental neuroscience · 2026Review
- GLUT1 and GLUT3 in brain glucose metabolism: mechanisms, regulation, and implications for metabolic disorders.Metabolic brain disease · 2025Review
- Neuroprotective effect of small extracellular vesicle-mediated targeting of AMPKα2 in cerebral ischemia.Metabolism: clinical and experimental · 2025Article
- Post-translational modifications orchestrate mTOR-driven cell death in cardiovascular disease.Frontiers in cardiovascular medicine · 2025Review
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Authors and funding
11 authors.
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Abstract
Neonatal hypoxic-ischemic encephalopathy (HIE) is the most common cause of death and long-term disabilities in term neonates. Caffeine exerts anti-inflammatory effects and has been used in neonatal intensive care units in recent decades. In our neonatal rat model of hypoxic-ischemic (HI) brain injury, we demonstrated that a single daily dose of caffeine (40 mg/kg) for 3 days post-HI reduced brain tissue loss and microgliosis compared to the vehicle group. The AMPK/mTOR pathway plays an important role in sensing the stress responses following brain injury. However, the role of mTOR in HI-associated brain damage remains unclear. A detailed analysis of the AMPK/mTOR pathway in our model revealed that this pathway plays a key role in hypoxia-regulated neuroprotection and can be significantly influenced by caffeine treatment. Targeting HI with caffeine might offer effective neuroprotection, reduce mortality, and improve functional outcomes in patients with HIE, especially in low- and middle-income countries, where neuroprotective treatment is urgently needed.
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