Evidence map›Paper›PMID 27812954›Full record

ReviewCurrent rheumatology reports2016

Activation of the Mechanistic Target of Rapamycin in SLE: Explosion of Evidence in the Last Five Years.

Zachary Oaks, Thomas Winans, Nick Huang, Katalin Banki, Andras Perl

Open access · greenAbstract readReview
In one paragraph

Review in Current rheumatology reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

50 citing papers in PubMed, 86 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Zachary OaksDepartment of Medicine, College of Medicine, State University of New York Upstate Medical University, 750 East Adams Street, Syracuse, NY, 13210, USA.
Thomas WinansDepartment of Medicine, College of Medicine, State University of New York Upstate Medical University, 750 East Adams Street, Syracuse, NY, 13210, USA.
Nick HuangDepartment of Medicine, College of Medicine, State University of New York Upstate Medical University, 750 East Adams Street, Syracuse, NY, 13210, USA.
Katalin BankiDepartment of Pathology, College of Medicine, State University of New York Upstate Medical University, Syracuse, NY, 13210, USA.
Andras PerlDepartment of Medicine, College of Medicine, State University of New York Upstate Medical University, 750 East Adams Street, Syracuse, NY, 13210, USA. perla@upstate.edu.
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
Endocytic Control of Autophagosome Formation in Lupus T cellsR01AI122176 · NIAID · UPSTATE MEDICAL UNIVERSITY · PI PERL, ANDRAS · 2016 to 2020
$2.0M
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
Treatment of Systemic Lupus Erythematosus (SLE) with N-acetylcysteine (NAC)R34AR068052 · NIAMS · UPSTATE MEDICAL UNIVERSITY · PI MCDERMOTT, MICHAEL P, PERL, ANDRAS · 2016 to 2017
$405k
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 R01 AI048079NIAID NIH HHS R01 AI072648NIAID NIH HHS R01 AI122176NIAID NIH HHS R56 AI048079NIAMS NIH HHS R34 AR068052NIDDK NIH HHS R01 DK078922
6 · The paper itself

Abstract

The mechanistic target of rapamycin (mTOR) is a central regulator in cell growth, activation, proliferation, and survival. Activation of the mTOR pathway underlies the pathogenesis of systemic lupus erythematosus (SLE). While mTOR activation and its therapeutic reversal were originally discovered in T cells, recent investigations have also uncovered roles in other cell subsets including B cells, macrophages, and "non-immune" organs such as the liver and the kidney. Activation of mTOR complex 1 (mTORC1) precedes the onset of SLE and associated co-morbidities, such as anti-phospholipid syndrome (APS), and may act as an early marker of disease pathogenesis. Six case reports have now been published that document the development of SLE in patients with genetic activation of mTORC1. Targeting mTORC1 over-activation with N-acetylcysteine, rapamycin, and rapalogs provides an opportunity to supplant current therapies with severe side effect profiles such as prednisone or cyclophosphamide. In the present review, we will discuss the recent explosion of findings in support for a central role for mTOR activation in SLE.

Indexed as

AcetylcysteineB-LymphocytesHumansImmunosuppressive AgentsLupus Erythematosus, SystemicSirolimusT-LymphocytesTOR Serine-Threonine KinasesAcetylcysteineImmunosuppressive AgentsMTOR protein, humanSirolimusTOR Serine-Threonine KinasesAnti-phospholipid antibodiesB cellsKidneyLiverMacrophagesMechanistic target of rapamycinMitochondriaSystemic lupus erythematosusT cells

Identifiers

PMID27812954
PMCPMC5314949
OpenAlexW2547741362

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.