Evidence map›Paper›PMID 24100461›Full record

ReviewNature reviews. Rheumatology2013

Oxidative stress in the pathology and treatment of systemic lupus erythematosus.

Andras Perl

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Rheumatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 213 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
213citing papers in PubMed, 4 pooled it
18.9field-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

213 citing papers in PubMed, 4 syntheses or guidelines pooled it, 349 citations in OpenAlex.

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  10. Autoinflammatory syndromes of STING and TREX1 dysfunction.The Journal of clinical investigation · 2026
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153 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 PerlDepartments of Medicine, Microbiology and Immunology, Biochemistry and Molecular Biology, Division of Rheumatology, State University of New York, 750 East Adams Street, Syracuse, NY 13210, USA.
State University of New York · US

Funding

SLE Treatment with N-acetylcysteineU01AR076092 · NIAMS · UPSTATE MEDICAL UNIVERSITY · PI Michael P McDermott, Andras Perl · 2020 to 2026
$7.9M
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
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 AT004332NCCIH NIH HHS R01 AT004332NIAID NIH HHS AI 048,079NIAID NIH HHS AI 072,648NIAID NIH HHS R01 AI048079NIAID NIH HHS R01 AI072648NIAMS NIH HHS U01 AR076092
6 · The paper itself

Abstract

Oxidative stress is increased in systemic lupus erythematosus (SLE), and it contributes to immune system dysregulation, abnormal activation and processing of cell-death signals, autoantibody production and fatal comorbidities. Mitochondrial dysfunction in T cells promotes the release of highly diffusible inflammatory lipid hydroperoxides, which spread oxidative stress to other intracellular organelles and through the bloodstream. Oxidative modification of self antigens triggers autoimmunity, and the degree of such modification of serum proteins shows striking correlation with disease activity and organ damage in SLE. In T cells from patients with SLE and animal models of the disease, glutathione, the main intracellular antioxidant, is depleted and serine/threonine-protein kinase mTOR undergoes redox-dependent activation. In turn, reversal of glutathione depletion by application of its amino acid precursor, N-acetylcysteine, improves disease activity in lupus-prone mice; pilot studies in patients with SLE have yielded positive results that warrant further research. Blocking mTOR activation in T cells could conceivably provide a well-tolerated and inexpensive alternative approach to B-cell blockade and traditional immunosuppressive treatments. Nevertheless, compartmentalized oxidative stress in self-reactive T cells, B cells and phagocytic cells might serve to limit autoimmunity and its inhibition could be detrimental. Antioxidant therapy might also be useful in ameliorating damage caused by other treatments. This Review thus seeks to critically evaluate the complexity of oxidative stress and its relevance to the pathogenesis and treatment of SLE.

Indexed as

Lupus Erythematosus, SystemicAnimalsAntioxidantsAutoimmunityHumansOxidative StressAntioxidants

Identifiers

PMID24100461
PMCPMC4046645
OpenAlexW2078472057

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.