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Activation of Piezo1-mediated mechanotransduction by LOX promotes neuronal ferroptosis leading to HIBD and discovery of LOX inhibitor TA

ABSTRACT: Neonatal hypoxic-ischemic brain damage (HIBD) is initiated by perinatal asphyxia, leading to brain injury triggered by reduced blood and oxygen flow, resulting in neurological impairments such as cerebral palsy, epilepsy, cognitive deficits, and behavioral disorders.Recent insights collectively suggest the important roles of lysyl oxidase (LOX) in the pathological processes of several acute and chronic neurological diseases, but the molecular regulatory mechanisms in HIBD remain elusive.In this study, we found through the study of HIBD rat models and the oxygen-glucose deprivation/re-oxygenation (OGD/R) cell models that LOX significantly increased after HIBD or OGD/R. RNA seq results showed a significant increase in piezo1 after primary neuron OGD/R, and iron death data was also enriched. Moreover, inhibiting LOX or piezo1 can rescue neuronal ferroptosis and further improve cognitive function in rats. In addition, we also found that traumatic acid can inhibit the enzyme activity of LOX and improve a series of pathological features of neuronal damage caused by increased LOX.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE270560 | GEO | 2024/09/25

REPOSITORIES: GEO

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Activation of Piezo1-mediated mechanotransduction by LOX promotes neuronal ferroptosis leading to HIBD and discovery of LOX inhibitor TA

Project description:Activation of Piezo1-mediated mechanotransduction by LOX promotes neuronal ferroptosis leading to HIBD and discovery of LOX inhibitor TA

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