Bilirubin enhances the activity of ASIC channels to exacerbate neurotoxicity in neonatal hyperbilirubinemia in mice

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Science Translational Medicine  12 Feb 2020:
Vol. 12, Issue 530, eaax1337
DOI: 10.1126/scitranslmed.aax1337

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Targeting acidity in jaundice

Neonatal hyperbilirubinemia, also called jaundice, is a pediatric condition caused by high bilirubin levels. When associated with acidosis, jaundice can trigger neurotoxicity and lead to neurological impairments. Now, Lai et al. investigated the link between acidosis and jaundice in human samples and animal models. In samples from children with concomitant acidosis and jaundice, neuronal injury was increased compared with children with jaundice and no acidosis. In mice, bilirubin potentiated the activity of acid-sensing ion channels (ASICs) in neurons, increased firing, and caused cell death. Hyperbilirubinemia and acidosis promoted cognitive impairments in mice that were prevented by ASIC deletion. Targeting ASICs might reduce neurological impairments associated with jaundice.

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