Evidence map›Paper›PMID 29518028›Full record

ReviewInternational journal of molecular sciences2018

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

Jessica Lawrence, Richard Nho

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05237687 (Sirolimus in Older Adults- Randomized Trial Assessing the Improvement in Phenotypic/Functional Biomarkers of Aging), which is not on this map. Cited by 98 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed, 1 pooled it
13.6field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT05237687 phase2recruitingnot on this mapstarted 2026, after this paper: background citation

Sirolimus in Older Adults- Randomized Trial Assessing the Improvement in Phenotypic/Functional Biomarkers of Aging

TypeinterventionalSponsorIrina TimofteRan2026 to 2028Enrolled10ConditionsAgingArmsSirolimus
3 · Its place in the literature

Who cites it

98 citing papers in PubMed, 1 synthesis or guideline pooled it, 184 citations in OpenAlex.

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38 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Jessica LawrenceDepartment of Veterinary Clinical Sciences, College of Veterinary Medicine & Masonic Cancer Center, University of Minnesota, St. Paul, MN 55108, USA. jlawrenc@umn.edu.ORCID 0000-0002-8315-1909
Richard NhoDivision of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine, University of Minnesota, 420 Delaware SE, Minneapolis, MN 55455, USA. nhoxx002@umn.edu.
University of Minnesota · US

Funding

Pathological alteration of FoxO3a in IPF pathogenesisR01HL114662 · NHLBI · UNIVERSITY OF MINNESOTA · PI NHO, RICHARD S. · 2013 to 2016
$1.5M
NHLBI NIH HHS R01 HL114662
6 · The paper itself

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.

Indexed as

AnimalsHumansPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-aktPulmonary FibrosisSignal TransductionTOR Serine-Threonine KinasesPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinasesfibrosisidiopathic pulmonary fibrosis (IPF)mammalian target of rapamycin (mTOR)phosphoinositide 3-kinase (PI3K)protein kinase B (AKT)radiation-induced pulmonary fibrosis (RIPF)

Identifiers

PMID29518028
PMCPMC5877639
OpenAlexW2793302312

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.