TREM-1 Attenuates RIPK3-mediated Necroptosis in Hyperoxia-induced Lung Injury in Neonatal Mice

What is it about?

Hyperoxia-induced inflammation and alveolar damage are critical contributors to acute lung injury and the development of bronchopulmonary dysplasia (BPD), the mechanisms of which have not been fully characterized. We show that triggering receptor expressed on myeloid cells 1 (TREM-1) functions by attenuating necroptosis and NLRP3-inflammation in neonatal lungs exposed to hyperoxia and identify TREM-1, Angiopoetin1, and RIPK3 as potential therapeutic targets for the treatment of BPD

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