Fig. 4

Cellular and molecular mechanisms of mechanosensitive ion channel-mediated mechanotransduction in acute lung injury/acute respiratory distress syndrome (ALI/ARDS). A–D Roles and mechanisms of ENaC (A), Piezo1 (B), TRPV4 (C) and K2P channels (D) in regulating alveolar fluid clearance, alveolar epithelial/endothelial barrier function, inflammatory response and surfactant secretion of ALI/ARDS. ENaC epithelial sodium channels, TRPV4 transient receptor potential vanilloid 4, K2P channels two-pore domain potassium channels, TNF-α tumor necrosis factor-α, IL-1β interleukin-1β, p38MAPK p38 mitogen-activated protein kinase, ERK1/2 extracellular signal-related kinase 1 and 2, CaMKII calmodulin-dependent protein kinase II, FLN-A filamin A, ICAM-1 intercellular adhesion molecule 1, SRC/PYK2 sarcoma/protein tyrosine kinase 2, HIF-1α hypoxia-inducible factor 1α, EDN1/CXCL2 endothelin 1/CXL motif chemokine ligand 2, MMPs matrix metalloproteinases, PKC protein kinase c, eNOS endothelial nitric oxide synthase, ROS/RNS reactive oxygen/nitrogen species, SGK1 serum glucocorticoid regulated kinase1, AQP-5 aquaporin-5, SP-C surfactant protein c, ECM extracellular matrix, TLRs toll like receptors (figure created using BioRender.com)