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@ARTICLE{Bernis:274029,
      author       = {Bernis, Maria E and Burkard, Hannah and Bremer, Anna-Sophie
                      and Grzelak, Kora and Zweyer, Margit and Maes, Elke and
                      Nacarkucuk, Efe and Kaibel, Hanna and Hakvoort, Charlotte
                      and Müller, Andreas and Sabir, Hemmen},
      title        = {{T}he {N}europrotective {E}ffects of {C}affeine in a
                      {N}eonatal {H}ypoxia-{I}schemia {M}odel are {R}egulated
                      through the {AMPK}/m{TOR} {P}athway.},
      journal      = {International journal of biological sciences},
      volume       = {21},
      number       = {1},
      issn         = {1449-2288},
      address      = {Lake Haven, N.S.W. [u.a.]},
      publisher    = {Ivyspring International Publ.},
      reportid     = {DZNE-2025-00010},
      pages        = {251 - 270},
      year         = {2025},
      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.},
      keywords     = {Caffeine: pharmacology / Caffeine: therapeutic use /
                      Animals / Neuroprotective Agents: therapeutic use /
                      Neuroprotective Agents: pharmacology / TOR Serine-Threonine
                      Kinases: metabolism / Hypoxia-Ischemia, Brain: metabolism /
                      Hypoxia-Ischemia, Brain: drug therapy / Rats / Animals,
                      Newborn / Rats, Sprague-Dawley / AMP-Activated Protein
                      Kinases: metabolism / Signal Transduction: drug effects /
                      Disease Models, Animal / AMPK (Other) / Caffeine (Other) /
                      Hypoxia-Ischemia (Other) / Neonatal (Other) /
                      Neuroprotection (Other) / mTOR (Other) / Caffeine (NLM
                      Chemicals) / Neuroprotective Agents (NLM Chemicals) / TOR
                      Serine-Threonine Kinases (NLM Chemicals) / AMP-Activated
                      Protein Kinases (NLM Chemicals)},
      cin          = {AG Sabir / AG Salomoni},
      ddc          = {570},
      cid          = {I:(DE-2719)5000032 / I:(DE-2719)1013032},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39744433},
      pmc          = {pmc:PMC11667826},
      doi          = {10.7150/ijbs.101087},
      url          = {https://pub.dzne.de/record/274029},
}