Fig. 3
From: Signaling pathways and potential therapeutic targets in acute respiratory distress syndrome (ARDS)
Schematic representation of the signaling pathways involved in epithelial and endothelial barrier regulation. During ARDS, the destructive signaling pathways that favor alveolar-capillary barrier disruption are predominant (left), whereas the protective signaling pathways that strengthen barrier integrity are downregulated (right), tilting the balance towards barrier disruption. Together, these result in increased alveolar-capillary permeability. AJs, adherens junctions; AKT, protein kinase B; ALK1, activin receptor-like kinase 1; Ang1, angiopoietin 1; BMP9, bone morphogenetic protein 9; cAMP, cyclic adenosine monophosphate; CREB, cyclic adenosine monophosphate response element binding; Drp1, dynamin-related protein 1; HIF-2α, hypoxia-inducible factor-2α; HMGB1, high-mobility group box 1; IL-1βR, interleukin-1β receptor; JAMs, junctional adhesion molecules; LPS, lipopolysaccharide; MLC, myosin light chain; P, phosphorylate; PI3K, phosphatidylinositol 3-kinase; RAGE, receptor for advanced glycation end products; Robo4, Roundabout 4; ROCK, Rho-associated protein kinase; S1P, sphingosine-1 phosphate; Smad, small mothers against decapentaplegic; Src, Src kinase; TJs, tight junctions; TLR, toll-like receptors; TRPV1, transient receptor potential‑vanilloid 1; VE-PTP, vascular endothelial protein tyrosine phosphatase; YAP, yes-associated protein; ZO-1, zonula occluden-1