The Role of the Mammalian Target of Rapamycin in Pulmonary Fibrosis

The review discussed the role of the mammalian target of rapamycin (mTOR) in pulmonary fibrosis, particularly in idiopathic pulmonary fibrosis (IPF) and radiation-induced pulmonary fibrosis (RIPF). It highlighted mTOR's involvement in cell metabolism, proliferation, differentiation, and survival, with dysregulation contributing to autophagy, inflammation, and cell growth issues leading to fibrosis. mTOR inhibitors, such as rapamycin, showed promise in reducing fibrosis in mouse models by decreasing fibrotic foci and inflammatory cell infiltrates. The review emphasized the need for effective therapies, as current treatments only reduce clinical exacerbations without curing the disease. Targeting mTOR, particularly its complexes mTORC1 and mTORC2, was suggested as a potential therapeutic strategy, given their roles in fibroblast proliferation, survival, and collagen production. The document also noted the complex interactions between mTOR, TGF-β, and other signaling pathways in promoting fibrosis, suggesting that mTOR modulation could offer novel therapeutic opportunities.