In sepsis-induced ALI/ARDS, MSCs (e.g., TRPV4) can be directly activated by several bacterial toxins (e.g., LPS) and indirectly activated by elevated oxidative stress (e.g., ROS) and pro-inflammatory mediators, and dysregulation of MSC-mediated mechanotransduction contribute to the pathogenesis (e.g., disruption of alveolar epithelia/endothelial barrier function) of sepsis-induce ALI/ARDS [42, 60]. Here, TRPV4 is linked to Sepsis.