The Akt inhibitor, triciribine, ameliorates chronic hypoxia‐induced vascular pruning and TGFβ‐induced pulmonary fibrosis

Interstitial lung disease accounts for a group of chronic and progressive disorders associated with severe pulmonary vascular remodelling, peripheral vascular rarefaction and fibrosis, thus limiting lung function. We have previously shown that Akt is necessary for myofibroblast differentiation, a critical event in organ fibrosis. However, the contributory role of the Akt‐mTOR pathway in interstitial lung disease and the therapeutic benefits of targeting Akt and mTOR remain unclear.