Cells, Volume 14, Issue 8
2025 April-2 - 64 articles
Cover Story: Hypoxic–ischemic encephalopathy (HIE) causes infant death and chronic disability. Therapeutic hypothermia (HT) is used clinically in some infant HIE, but cooled HIE babies grow up with persisting brain damage and cognitive, motor, and social deficits. Martin et al. studied postmortem human neonatal HIE cases with or without HT, newborn pig HIE models, and human stem cell models. They found that the mode of degeneration shifted from necrosis to apoptosis–necrosis hybrid and apoptotic forms in human HIE-HT, whereas neurons in piglet HIE-HT were unshifting and salvaged. Toxic conformer proteinopathy (TCP) occurred in HIE brains involving α-synuclein and superoxide dismutase-1 and was replicated in human cell models. TCP occurred in human HIE regardless of HT but was mitigated in HT piglets. TCP could drive the evolution and persistence of HIE across the lifespan. View this paper - Issues are regarded as officially published after their release is announced to the table of contents alert mailing list .
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