PMID- 29518028
OWN - NLM
STAT- MEDLINE
DCOM- 20180814
LR  - 20211204
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 19
IP  - 3
DP  - 2018 Mar 8
TI  - The Role of the Mammalian Target of Rapamycin (mTOR) in Pulmonary Fibrosis.
LID - 10.3390/ijms19030778 [doi]
LID - 778
AB  - 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.
FAU - Lawrence, Jessica
AU  - Lawrence J
AUID- ORCID: 0000-0002-8315-1909
AD  - Department of Veterinary Clinical Sciences, College of Veterinary Medicine & 
      Masonic Cancer Center, University of Minnesota, St. Paul, MN 55108, USA. 
      jlawrenc@umn.edu.
FAU - Nho, Richard
AU  - Nho R
AD  - Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of 
      Medicine, University of Minnesota, 420 Delaware SE, Minneapolis, MN 55455, USA. 
      nhoxx002@umn.edu.
LA  - eng
GR  - R01 HL114662/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Review
DEP - 20180308
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - 0 (Protein Kinase Inhibitors)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Animals
MH  - Humans
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Protein Kinase Inhibitors/*pharmacology/therapeutic use
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Pulmonary Fibrosis/drug therapy/*metabolism
MH  - Signal Transduction
MH  - TOR Serine-Threonine Kinases/antagonists & inhibitors/genetics/*metabolism
PMC - PMC5877639
OTO - NOTNLM
OT  - fibrosis
OT  - idiopathic pulmonary fibrosis (IPF)
OT  - mammalian target of rapamycin (mTOR)
OT  - phosphoinositide 3-kinase (PI3K)
OT  - protein kinase B (AKT)
OT  - radiation-induced pulmonary fibrosis (RIPF)
COIS- The authors declare no conflict of interest.
EDAT- 2018/03/09 06:00
MHDA- 2018/08/15 06:00
PMCR- 2018/03/01
CRDT- 2018/03/09 06:00
PHST- 2018/01/31 00:00 [received]
PHST- 2018/02/22 00:00 [revised]
PHST- 2018/03/06 00:00 [accepted]
PHST- 2018/03/09 06:00 [entrez]
PHST- 2018/03/09 06:00 [pubmed]
PHST- 2018/08/15 06:00 [medline]
PHST- 2018/03/01 00:00 [pmc-release]
AID - ijms19030778 [pii]
AID - ijms-19-00778 [pii]
AID - 10.3390/ijms19030778 [doi]
PST - epublish
SO  - Int J Mol Sci. 2018 Mar 8;19(3):778. doi: 10.3390/ijms19030778.