Knockout of Piezo1 strongly relieves the severity of lipopolysaccharide- induced VILI in rats with ARDS, and further experiments have shown that excessive mechanical stretching opens the Piezo1 channel, permits calcium ions to enter cells, stimulates calpain, disassembles beta-catenin, p120-catenin, and the VE-cadherin complex, induces the internalization and degradation of the VE-cadherin, breaks down the endothelial barrier, and finally induces lung injury (47). Here, CTNNB1 is linked to acute respiratory distress syndrome.