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The epithelial sodium channel (ENaC) is the driving force for pulmonary edema absorption in acute lung injury (ALI). Netrin-1 is a newly found anti-inflammatory factor that works by activating the adenosine 2B receptor (A2BAR). Meanwhile, activated A2BAR has the potential to enhance ENaC-dependent alveolar fluid clearance (AFC). However, whether netrin-1 can increase ENaC-mediated AFC by activating A2BAR remains unclear.

respiration

Netrin-1 Promotes Epithelial Sodium Channel-Mediated Alveolar Fluid Clearance via Activation of the Adenosine 2B Receptor in Lipopolysaccharide-Induced Acute Lung Injury