Englert Lab

Targeting mTORC1 activation during lung injury

Our lab recently discovered that the mechanistic target of rapamycin complex 1 (mTORC1) functions as a mechanosensor in lung epithelial cells during mechanical ventilation. In contrast to canonical activation of the mTORC1 pathway under favorable growth conditions, activation of mTORC1 during injurious ventilation induces surfactant dysfunction that perpetuates lung injury. We use genetically-modified mice, preclinical ARDS models, and microfluidic models of the lung microenvironment to determine the mechanisms by which mTORC1 activation drives lung injury during the acute respiratory distress syndrome (ARDS) and ventilator induced lung injury (VILI).

Relevant publications:

mTORC1 is a mechanosensor that regulates surfactant function and lung compliance during ventilator-induced lung injury