Evidence map›Paper›PMID 25907074›Full record

ReviewAnnals of the New York Academy of Sciences2015

mTOR activation is a biomarker and a central pathway to autoimmune disorders, cancer, obesity, and aging.

Andras Perl

Open access · greenAbstract readReview
In one paragraph

Review in Annals of the New York Academy of Sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed
11.9field-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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

117 citing papers in PubMed, 214 citations in OpenAlex.

  1. Curcumin (The Journal of clinical and aesthetic dermatology · 2026
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  8. The role of mTOR activation in steroid-resistant asthma: insights from particulate matter-induced mouse model and patient studies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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57 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

1 author at 1 institution in 1 country.

Andras PerlDivision of Rheumatology, Department of Medicine State University of New York, Upstate Medical University, College of Medicine, Syracuse, New York.
SUNY Upstate Medical University · US

Funding

Metabolic Control of T-cell Lineage Specification in SLER01AI072648 · NIAID · UPSTATE MEDICAL UNIVERSITY · PI PERL, ANDRAS · 2008 to 2024
$6.1M
IMPACT OF HRES-1 ENDOGENOUS RETROVIRUS IN SLER01AI048079 · NIAID · UPSTATE MEDICAL UNIVERSITY · PI PERL, ANDRAS · 2000 to 2013
$2.7M
Treatment of SLE with N-acetylcysteineR01AT004332 · NCCIH · UPSTATE MEDICAL UNIVERSITY · PI PERL, ANDRAS · 2008 to 2011
$1.6M
Pathogenesis and Treatment of Liver Disease in Transaldolase DeficiencyR01DK078922 · NIDDK · UPSTATE MEDICAL UNIVERSITY · PI PERL, ANDRAS · 2010 to 2013
$1.4M
MOLECULAR BIOLOGY OF TRANSALDOLASER01DK049221 · NIDDK · UPSTATE MEDICAL UNIVERSITY · PI PERL, ANDRAS · 1996 to 2004
$904k
Genetic and Immunological Impact of the HRES-1/Rab4 Locus in SLER56AI048079 · NIAID · UPSTATE MEDICAL UNIVERSITY · PI PERL, ANDRAS · 2008 to 2008
$275k
NCCIH NIH HHS R01 AT004332NIAID NIH HHS AI 048079 ANDNIAID NIH HHS AI 072648NIAID NIH HHS R01 AI048079NIAID NIH HHS R01 AI072648NIAID NIH HHS R56 AI048079NIDDK NIH HHS R01 DK049221NIDDK NIH HHS R01 DK078922
6 · The paper itself

Abstract

The mechanistic target of rapamycin (mTOR) is a ubiquitous serine/threonine kinase, which plays pivotal roles in integrating growth signals on a cellular level. To support proliferation and survival under stress, two interacting complexes that harbor mTOR, mTORC1 and mTORC2, promote the transcription of genes involved in carbohydrate metabolism and lipogenesis, enhance protein translation, and inhibit autophagy. Although rapamycin was originally developed as an inhibitor of T cell proliferation for preventing organ transplant rejection, its molecular target, mTOR, has been subsequently identified as a central regulator of metabolic cues that drive lineage specification in the immune system. Owing to oxidative stress, the activation of mTORC1 has emerged as a central pathway for the pathogenesis of systemic lupus erythematosus and other autoimmune diseases. Paradoxically, mTORC1 has also been identified as a mediator of the Warburg effect that allows cell survival under hypoxia. Rapamycin and new classes of mTOR inhibitors are being developed to block not only transplant rejection and autoimmunity but also to treat obesity and various forms of cancer. Through preventing these diseases, personalized mTOR blockade holds promise to extend life span.

Indexed as

AgingAnimalsAutoimmune DiseasesBiomarkersHumansNeoplasmsObesityPrecision MedicineSignal TransductionSirolimusTOR Serine-Threonine KinasesBiomarkersMTOR protein, humanSirolimusTOR Serine-Threonine Kinasesautoimmunityautophagybiomarkerglutathioneglycolysishypoxiainflammationkeloid diseasekynureninemetabolismmitochondriamTORoxidative stresspathogenesispentose phosphate pathwayrapamycinsirolimussystemic lupus erythematosusT cell activationtreatment

Identifiers

PMID25907074
PMCPMC4480196
OpenAlexW1749413658

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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 OpenQuestion graph.