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Idiopathic Pulmonary Fibrosis (IPF) is usually a devastating disease, which afflicts over 200,000 individuals in the United states and Europe [1]. The pathogenesis is unknown but a dysregulated wound healing response to lung epithelial injury, which results in progressive interstitial fibrosis, is really a hallmark in the disease. Activated fibroblasts in fibroblastic foci secrete various profibrotic proteins in response to TGF-b, for example form I and sort III collagen, fibronectin (FN), plus the matricellular members of the family, secreted protein acidic and wealthy in cysteine (SPARC) and connected tissue development factor (CTGF) [2]. The evolutionary conserved serine/threonine protein kinase mTOR can be a member of your phosphatidylinositol 3-kinase (PI3K)connected kinase (PIKK) household [3]. mTOR integrates both extracellular and intracellular signals and acts as a central regulator of cell metabolism, growth, proliferation and survival [4]. In mammalian cells, mTOR resides in two physically and functionally distinct signaling complexes: mTOR complicated 1 (mTORC1), a rapamycin-sensitive complicated, and mTOR complex two (mTORC2) [5,6]. The mTORC1 complicated consists of at least 5 components: (i) mTOR, the catalytic subunit with the complicated; (ii) Raptor; (iii) mLS8; (iv) PRAS40; and (v) Deptor; mTORC1 phosphorylates the ribosomal S6K1 (protein S6 kinase 1) and 4EPLOS A single | plosone.orgBP1 (eukaryotic translation initiation element eIF4E binding protein 1) proteins, which regulate growth and protein synthesis, respectively [7]. Rapamycin and related rapalogs are recognized allosteric inhibitors of mTORC1 but do not usually directly inhibit mTORC2, though prolonged therapy with rapam.