Deletion of ASK1 Protects against Hyperoxia-Induced Acute Lung Injury
作者： Jutaro Fukumoto , Ruan Cox , Itsuko Fukumoto , Young Cho , Prasanna Tamarapu Parthasarathy
DOI: 10.1371/JOURNAL.PONE.0147652
关键词:
摘要: Apoptosis signal-regulating kinase 1 (ASK1), a member of the MAPK (MAP3K) family, is activated by various stimuli, which include oxidative stress, endoplasmic reticulum (ER) calcium influx, DNA damage-inducing agents and receptor-mediated signaling through tumor necrosis factor receptor (TNFR). Inspiration high concentration oxygen palliative therapy counteracts hypoxemia caused acute lung injury (ALI)-induced pulmonary edema. However, animal experiments so far have shown that hyperoxia itself could exacerbate ALI reactive species (ROS). Our previous data indicates ASK1 plays pivotal role in hyperoxia-induced (HALI). it unclear whether or not deletion vivo protects against HALI. In this study, we investigated would lead to attenuation results show significantly suppresses elevation inflammatory cytokines (i.e. IL-1β TNF-α), cell apoptosis lung, recruitment immune cells. summary, from study suggest mice inhibits hyperoxic injury.
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