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@ARTICLE{Nacarkucuk:272509,
      author       = {Nacarkucuk, Efe and Bernis, Maria E. and Bremer,
                      Anna-Sophie and Grzelak, Kora and Zweyer, Margit and Maes,
                      Elke and Burkard, Hannah and Sabir, Hemmen},
      title        = {{N}europrotective {E}ffect of {M}elatonin in a {N}eonatal
                      {H}ypoxia–{I}schemia {R}at {M}odel {I}s {R}egulated by the
                      {AMPK}/m{TOR} {P}athway},
      journal      = {Journal of the American Heart Association},
      volume       = {13},
      number       = {19},
      issn         = {2047-9980},
      address      = {New York, NY},
      publisher    = {Association},
      reportid     = {DZNE-2024-01185},
      pages        = {e036054},
      year         = {2024},
      abstract     = {Melatonin has been shown to be neuroprotective in different
                      animal models of neonatal hypoxic-ischemic brain injury.
                      However, its exact molecular mechanism of action remains
                      unknown. Our aim was to prove melatonin's short- and
                      long-term neuroprotection and investigate its role on the
                      AMPK (AMP-activated protein kinase)/mTOR (mammalian target
                      of rapamycin) pathway following neonatal hypoxic-ischemic
                      brain injury.Seven-day-old Wistar rat pups were exposed to
                      hypoxia-ischemia, followed by melatonin or vehicle
                      treatment. Detailed analysis of the AMPK/mTOR/autophagy
                      pathway, short- and long-term neuroprotection, myelination,
                      and oligodendrogenesis was performed at different time
                      points. At 7 days after hypoxia-ischemia, melatonin-treated
                      animals showed a significant decrease in tissue loss,
                      increased oligodendrogenesis, and myelination. Long-term
                      neurobehavioral results showed significant motor improvement
                      following melatonin treatment. Molecular pathway analysis
                      showed a decrease in the AMPK expression, with a significant
                      increase at mTOR's downstream substrates, and a significant
                      decrease at the autophagy marker levels in the melatonin
                      group compared with the vehicle group.Melatonin treatment
                      reduced brain area loss and promoted oligodendrogenesis with
                      a clear improvement of motor function. We found that
                      melatonin associated neuroprotection is regulated via the
                      AMPK/mTOR/autophagy pathway. Considering the beneficial
                      effects of melatonin and the results of our study, melatonin
                      seems to be an optimal candidate for the treatment of
                      newborns with hypoxic-ischemic brain injury in high- as well
                      as in low- and middle-income countries.},
      keywords     = {Animals / Melatonin: pharmacology / Hypoxia-Ischemia,
                      Brain: metabolism / Hypoxia-Ischemia, Brain: drug therapy /
                      Hypoxia-Ischemia, Brain: pathology / TOR Serine-Threonine
                      Kinases: metabolism / Animals, Newborn / Rats, Wistar /
                      Neuroprotective Agents: pharmacology / Disease Models,
                      Animal / Signal Transduction: drug effects / AMP-Activated
                      Protein Kinases: metabolism / AMP-Activated Protein Kinases:
                      drug effects / Autophagy: drug effects / Oligodendroglia:
                      drug effects / Oligodendroglia: metabolism /
                      Oligodendroglia: pathology / Brain: drug effects / Brain:
                      metabolism / Brain: pathology / Rats / Behavior, Animal:
                      drug effects / AMPK/mTOR/autophagy (Other) / melatonin
                      (Other) / neonatal hypoxia–ischemia (Other) /
                      neuroprotection (Other) / rat (Other) / Melatonin (NLM
                      Chemicals) / TOR Serine-Threonine Kinases (NLM Chemicals) /
                      Neuroprotective Agents (NLM Chemicals) / mTOR protein, rat
                      (NLM Chemicals) / AMP-Activated Protein Kinases (NLM
                      Chemicals)},
      cin          = {AG Sabir / AG Salomoni},
      ddc          = {610},
      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},
      pmc          = {pmc:PMC11681444},
      pubmed       = {pmid:39319465},
      doi          = {10.1161/JAHA.124.036054},
      url          = {https://pub.dzne.de/record/272509},
}