Unveiling the Emerging Role of Extracellular Vesicle–Inflammasomes in Hyperoxia-Induced Neonatal Lung and Brain Injury

Cells, Journal Year: 2024, Volume and Issue: 13(24), P. 2094 - 2094

Published: Dec. 18, 2024

Extremely premature infants are at significant risk for developing bronchopulmonary dysplasia (BPD) and neurodevelopmental impairment (NDI). Although BPD is a predictor of poor outcomes, it currently unknown how contributes to brain injury long-term NDI in pre-term infants. Extracellular vesicles (EVs) small, membrane-bound structures released from cells into the surrounding environment. EVs involved inter-organ communication diverse pathological processes. Inflammasomes large, multiprotein complexes that part innate immune system responsible triggering inflammatory responses cell death. Apoptosis-associated speck-like protein containing caspase recruitment domain (ASC) pivotal inflammasome assembly activating caspase-1. Activated caspase-1 cleaves gasdermin D (GSDMD) release 30 kD N-terminal can form membrane pores, leading lytic death, also known as pyroptosis. cleave pro-IL-1β pro-IL-18 their active forms, which be rapidly through GSDMD pores induce inflammation. Recent evidence has emerged activation inflammasomes associated with neonatal lung injury, inhibition reduces hyperoxia-induced injury. Additionally, multiple studies have demonstrated hyperoxia stimulates lung-derived contain cargos. Adoptive transfer these circulation normal mice rats induces This review focuses on EV–inflammasomes’ roles mediating lung-to-brain crosstalk via EV-dependent EV-independent mechanisms critical BPD, pathogenesis. EV–inflammasomes will discussed potential therapeutic targets

Language: Английский

MicroRNA Expression Profiles in the Neonatal Rat Hippocampus Exposed to Normobaric Hyperoxia

Open Journal of Pediatrics, Journal Year: 2024, Volume and Issue: 14(06), P. 1038 - 1049

Published: Jan. 1, 2024

Language: Английский