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Int. J. Mol. Sci. 2018, 19(3), 778; https://doi.org/10.3390/ijms19030778

The Role of the Mammalian Target of Rapamycin (mTOR) in Pulmonary Fibrosis

1
Department of Veterinary Clinical Sciences, College of Veterinary Medicine & Masonic Cancer Center, University of Minnesota, St. Paul, MN 55108, USA
2
Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine, University of Minnesota, 420 Delaware SE, Minneapolis, MN 55455, USA
*
Author to whom correspondence should be addressed.
Received: 31 January 2018 / Revised: 22 February 2018 / Accepted: 6 March 2018 / Published: 8 March 2018
(This article belongs to the Special Issue Cell Growth Regulation)
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Abstract

The phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR)-dependent pathway is one of the most integral pathways linked to cell metabolism, proliferation, differentiation, and survival. This pathway is dysregulated in a variety of diseases, including neoplasia, immune-mediated diseases, and fibroproliferative diseases such as pulmonary fibrosis. The mTOR kinase is frequently referred to as the master regulator of this pathway. Alterations in mTOR signaling are closely associated with dysregulation of autophagy, inflammation, and cell growth and survival, leading to the development of lung fibrosis. Inhibitors of mTOR have been widely studied in cancer therapy, as they may sensitize cancer cells to radiation therapy. Studies also suggest that mTOR inhibitors are promising modulators of fibroproliferative diseases such as idiopathic pulmonary fibrosis (IPF) and radiation-induced pulmonary fibrosis (RIPF). Therefore, mTOR represents an attractive and unique therapeutic target in pulmonary fibrosis. In this review, we discuss the pathological role of mTOR kinase in pulmonary fibrosis and examine how mTOR inhibitors may mitigate fibrotic progression. View Full-Text
Keywords: fibrosis; mammalian target of rapamycin (mTOR); idiopathic pulmonary fibrosis (IPF); radiation-induced pulmonary fibrosis (RIPF); phosphoinositide 3-kinase (PI3K); protein kinase B (AKT) fibrosis; mammalian target of rapamycin (mTOR); idiopathic pulmonary fibrosis (IPF); radiation-induced pulmonary fibrosis (RIPF); phosphoinositide 3-kinase (PI3K); protein kinase B (AKT)
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).
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Lawrence, J.; Nho, R. The Role of the Mammalian Target of Rapamycin (mTOR) in Pulmonary Fibrosis. Int. J. Mol. Sci. 2018, 19, 778.

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