Fig. 4.

Schematic representation of the signaling pathways that impair alveolar fluid clearance during ARDS. AKT, protein kinase B; AMPK, AMP-activated protein kinase; AT 1, Angiotensin II receptor 1; CAMKK-β, Ca²⁺/calmodulin-dependent kinase kinase-β; cAMP, cyclic adenosine monophosphate; CFTR, cystic fibrosis transmembrane conductance regulator; ENaC, epithelial Na⁺ channel; HMGB1, high-mobility group box 1; IL-1β, interleukin-1β; IL-1βR, interleukin-1β receptor; MyD88, myeloid differentiation primary response gene 88; Na,K-ATPase, sodium–potassium adenosine triphosphatase; Nedd4-2, neuronal precursor cell expressed developmentally down-regulated protein4-2; p38MAPK, p38 mitogen-activated protein kinase; PI3K, phosphatidylinositol 3-kinase; PKC-ζ, protein kinase C-ζ; RAGE, receptor for advanced glycation end product; Smad, small mothers against decapentaplegic; TGF-β, transforming growth factor-β; TGF-βR, transforming growth factor-β receptor; TRAIL, TNF-related apoptosis-inducing ligand; TRAILR, TNF-related apoptosis-inducing ligand receptor