Fig. 3.

SACs as orchestrators of alveolar inflammation in ARDS. Hyperoxia, mechanical stretch, and inflammatory cytokines alter SAC expression and function, which impacts the pathogenesis of ARDS through downstream effects on cytokine secretion from epithelial, endothelial, inflammatory, and immune cells and alveolar-capillary barrier function (epithelial and endothelial cells). While some of these processes are mediated via changes in intracellular Ca²⁺ concentrations ([Ca_i²⁺]), others appear Ca²⁺ independent.