Patients suffering from acute respiratory distress syndrome (ARDS) require mechanical ventilation in order to maintain adequate gas exchange. However, ventilation can contribute to further lung damage through overdistension and/or the reopening of fluid-filled airways which causes epithelial cell (EpC) death and detachment and an upregulated inflammatory response [1]. While previous research has focused on minimizing the injurious mechanical forces generated during ventilation [2], an alternative approach is to alter the way that forces are transmitted from the cell surface to its structural elements (cell membrane, cytoskeleton, focal adhesions, cell-cell attachments). One way to alter force transmission is to alter the cell’s intrinsic biomechanical or biostructural properties. For example, our lab has previously shown that depolymerization of the actin cytoskeletal structure can reduce cell necrosis during airway reopening [3].

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